bims-celmim Biomed News
on Cellular and mitochondrial metabolism
Issue of 2025–09–21
twenty-six papers selected by
Marc Segarra Mondejar



  1. Oncogene. 2025 Sep 16.
      Although the involvement of polo-like kinase 1 (PLK1) in metabolic reprogramming from oxidative phosphorylation (OXPHOS) to glycolysis has been previously described, the underlying molecular mechanism remains unclear. Pyruvate dehydrogenase (PDH) catalyzes the conversion of pyruvate into acetyl-CoA, the starting material for the tricarboxylic acid (TCA) cycle. In a companion study by Zhang et al., we demonstrated that PLK1 phosphorylation of PDHA1 at threonine 57 (PDHA1-T57) drives its protein degradation via mitophagy activation. Using a stable-isotope resolved metabolomics (SIRM) approach, we now show that PLK1 phosphorylation of PDHA1-T57 results in metabolic reprogramming from OXPHOS to glycolysis. Notably, cells mimicking PDHA1-T57 phosphorylation rely more on the aspartate-malate shuttle than on glucose-derived pyruvate to sustain the TCA cycle. This metabolic shift was also observed in mouse embryonic fibroblasts (MEFs) and transgenic mice conditionally expressing the PDHA1-T57D variant, highlighting the role of PLK1 in metabolic reprogramming in vivo. It is well-established that pyruvate dehydrogenase kinase (PDK)-mediated phosphorylation of PDH leads to its inactivation and that dichloroacetic acid (DCA), a PDK inhibitor, has been investigated in preclinical and early clinical studies as a potential therapeutic agent for lung cancer. We demonstrated that DCA combined with Onvansertib, a PLK1 inhibitor, synergistically inhibits lung tumor growth by enhancing mitochondrial ROS, inhibiting glycolysis, and inducing apoptosis. This study aims to elucidate how PLK1-associated activity drives the metabolic reprogramming from OXPHOS to glycolysis during cellular transformation, thereby contributing to lung carcinogenesis. Our results provide support for a clinical trial to evaluate the efficacy of Onvansertib plus DCA in treating lung cancer.
    DOI:  https://doi.org/10.1038/s41388-025-03571-1
  2. EMBO J. 2025 Sep 16.
      Cellular metabolism plays a pivotal role in regulating the effector functions and fate decisions of immune cells, shaping immune responses in homeostasis and disease. Metabolic pathways also serve as critical signaling hubs governing immune cell behavior. Deregulated metabolic pathways contribute to immune dysfunction, fueling disease progression and creating challenges for therapeutic interventions. The recent development of advanced technologies to delineate immunometabolic regulation has revolutionized our understanding of immune cell biology. These tools, ranging from quantitative single-cell metabolomics to in vivo spatial tissue profiling and DC-based metabolic therapy, have shifted the focus from broad nutrient pathways to a detailed exploration of metabolic reprogramming within disease microenvironments, revealing how metabolic changes drive immune cell activation, differentiation, and effector responses. The integration of immunometabolic insights into clinical practice holds strong potential for advancing precision medicine and developing targeted therapies that restore immune balance in pathological conditions. Here, we summarize emerging cutting-edge technologies related to immunometabolism and critically reflect on their current limitations. Finally, we discuss potential needs for developing novel methods that can uncover the intricate interplay between metabolism and immune cell function.
    Keywords:  Dendritic Cells; Immunometabolism; Metabolic Reprogramming; T Cells; Technological Advances
    DOI:  https://doi.org/10.1038/s44318-025-00569-z
  3. Commun Biol. 2025 Sep 19. 8(1): 1348
      Ion transport within mitochondria influences their structure, energy production, and cell death regulation. TMBIM5, a conserved calcium/proton exchanger in the inner mitochondrial membrane, contributes to mitochondrial structure, ATP synthesis, and apoptosis regulation. The relationship of TMBIM5 with the mitochondrial calcium uniporter complex formed by MCU, MICU1-3, and EMRE remains undefined. We generated Tmbim5-deficient Drosophila that exhibit disrupted cristae architecture, premature mitochondrial permeability transition pore opening, reduced calcium uptake, and mitochondrial swelling - resulting in impaired mobility and shortened lifespan. Crossing these with flies lacking mitochondrial calcium uniporter complex proteins was generally detrimental, but partial MICU1 depletion ameliorated the Tmbim5-deficiency phenotype. In human cells, MICU1 rescues morphological defects in TMBIM5-knockout mitochondria, while TMBIM5 overexpression exacerbates size reduction in MICU1-knockout mitochondria. Both proteins demonstrated opposing effects on submitochondrial localization and coexisted in the same macromolecular complex. Our findings establish a functional interplay between TMBIM5 and MICU1 in maintaining mitochondrial integrity, with implications for understanding calcium homeostasis mechanisms.
    DOI:  https://doi.org/10.1038/s42003-025-08839-6
  4. FEBS Open Bio. 2025 Sep 19.
      Tryptophan (Trp) is the largest and most structurally complex amino acid, yet it is the least abundant in the proteome. Its distinct indole ring and high carbon content allow it to give rise to several biologically active metabolites, including serotonin, kynurenine (Kyn), and indole-3-pyruvate (I3P). Dysregulation of Trp metabolism has been implicated in a range of diseases, from depression to cancer. Investigating Trp and its metabolites in healthy tissues provides insight into how disease-associated disruptions may be targeted selectively while preserving essential physiological functions. Whereas previous studies have typically focused on individual organs or single metabolic branches, our analysis spans 12 peripheral organs, the central nervous system, and serum in male and female (C57BL/6) mice across three life stages: young (3 weeks), adult (54 weeks), and aged (74 weeks). We identified striking tissue-, sex-, and age-specific differences in Trp metabolism, including elevated levels of I3P and Kyn, both linked to tumor growth, in aging males. We also compared Trp metabolite profiles in tissues from mice fed a control defined diet versus a Trp-deficient diet for three weeks. This intervention led to a marked reduction in circulating Trp and its metabolites, with more modest effects observed in the liver and central nervous system. These findings underscore the importance of organ-specific and diet-sensitive analyses of Trp metabolism for understanding its role in both normal physiology and disease. Establishing baseline levels of Trp metabolites across tissues may also provide a foundation for identifying organ-specific metabolic reprogramming in cancer and other illnesses.
    Keywords:  atlas; indole‐3‐pyruvate; kynurenine; metabolism; serotonin; tryptophan
    DOI:  https://doi.org/10.1002/2211-5463.70123
  5. Trends Cancer. 2025 Sep 16. pii: S2405-8033(25)00204-3. [Epub ahead of print]
      The tumor microenvironment (TME) imposes profound metabolic and functional constraints on immune cells, with mitochondrial dysfunction emerging as a pivotal driver of immunosuppression. While mitochondrial metabolism is well recognized for its role in energy production and cellular homeostasis, its dynamic regulation of immune cell activation, differentiation, and exhaustion within the TME remains underexplored. In this review we summarize insights into how TME stressors such as hypoxia, nutrient competition, and metabolic byproducts subvert mitochondrial dynamics, redox balance, and mitochondrial DNA (mtDNA) signaling in T cells, natural killer (NK) cells, and macrophages, thereby directly impairing their antitumor efficacy. We emphasize that the restoration of mitochondrial fitness in immune cells, achieved by targeting metabolites in the TME and mitochondrial quality control, represents a pivotal axis for adoptive cell therapies (ACTs) and TME reprogramming.
    Keywords:  ROS; chimeric antigen receptor (CAR); metabolism; mitochondria; tumor immunotherapy
    DOI:  https://doi.org/10.1016/j.trecan.2025.08.006
  6. Cell Rep. 2025 Sep 15. pii: S2211-1247(25)01051-4. [Epub ahead of print]44(9): 116280
      Neurons and astrocytes play critical yet divergent roles in brain physiology and neurological conditions. Intracellular organelles are integral to cellular function. However, an in-depth characterization of organelles in live neural cells has not been performed. Here, we use multispectral imaging to simultaneously visualize six organelles-endoplasmic reticulum (ER), lysosomes, mitochondria, peroxisomes, Golgi, and lipid droplets-in live primary rodent neurons and astrocytes. We generate a dataset of 173 z stack and 98 time-lapse images, accompanied by quantitative "organelle signature" analysis. Comparative analysis reveals a clear cell-type specificity in organelle morphology and interactions. Neurons are characterized by prominent mitochondrial composition and interactions, while astrocytes contain more lysosomes and lipid droplet interactions. Additionally, neurons display a more robust organelle response than astrocytes to acute oxidative or ER stress. Our data provide a systems-level characterization of neuron and astrocyte organelles that can be a reference for understanding cell-type-specific physiology and disease.
    Keywords:  CP: Cell biology; CP: Neuroscience; Golgi; astrocytes; endoplasmic reticulum; lipid droplets; lysosomes; microscopy; mitochondria; neurons; organelles; peroxisomes
    DOI:  https://doi.org/10.1016/j.celrep.2025.116280
  7. Cell Rep Med. 2025 Sep 16. pii: S2666-3791(25)00429-X. [Epub ahead of print]6(9): 102356
      Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer, associated with poor response to therapies and high mortality. We identify that phosphodiesterase 7A (PDE7A) is overexpressed in the majority of TNBCs, and a higher level of PDE7A associates with poor prognosis. The phosphatidylinositol 3-kinase (PI3K)/AKT pathway, via the transcription factor IRF1, stimulates the expression of PDE7A in TNBC cells. PDE7A inhibition attenuates TNBC growth in both cell culture and mouse models of TNBC. Inhibition of PDE7A suppresses de novo pyrimidine biosynthesis, in part through the downregulation of the enzyme dihydroorotate dehydrogenase (DHODH). DHODH suppression attenuates TNBC tumor growth, mirroring the effects of PDE7A inhibition, and ectopic DHODH expression rescues PDE7A-inhibition-induced tumor suppression. Pharmacological co-targeting of PDE7A and DHODH potently inhibits TNBC tumor growth and metastasis. These findings identify the PDE7A → DHODH →de novo pyrimidine biosynthesis pathway as a key driver of TNBC, offering additional therapeutic opportunities for TNBC patients.
    Keywords:  DHODH; PDE7A; phosphodiesterases; pyrimidine biosynthesis; triple-negative breast cancer
    DOI:  https://doi.org/10.1016/j.xcrm.2025.102356
  8. Nat Chem Biol. 2025 Sep 15.
      The lipid composition of cells varies widely across organelles and between individual membrane leaflets. Transport proteins are thought to generate this heterogeneity, but measuring their functions in vivo has been hampered by limited tools for imaging lipids at relevant spatial resolutions. Here we present fluorogen-activating coincidence encounter sensing (FACES), a chemogenetic tool capable of quantitatively imaging subcellular lipid pools and reporting their transbilayer orientation in living cells. FACES combines bioorthogonal chemistry with genetically encoded fluorogen-activating proteins (FAPs) for reversible proximity sensing of conjugated molecules. We first apply this approach to identify roles for lipid transfer proteins that traffic phosphatidylcholine pools between the ER and mitochondria. We then show that transmembrane domain-containing FAPs can reveal the membrane asymmetry of multiple lipid classes in the trans-Golgi network and be used to investigate the mechanisms that generate it. Finally, we present that FACES can be applied to measure glycans and other molecule classes.
    DOI:  https://doi.org/10.1038/s41589-025-02021-z
  9. Cell Rep. 2025 Sep 12. pii: S2211-1247(25)01017-4. [Epub ahead of print]44(9): 116246
      We developed the AVID (ATP visualization in vivo directly) mouse, a genetically encoded biosensor mouse enabling real-time, multiscale imaging of ATP dynamics across the whole body, organs, and cellular compartments in living animals. AVID revealed previously undetectable localized ATP depletion near the central vein of the liver after myocardial infarction, spatially linked to kynurenic acid accumulation-a phenomenon invisible to conventional bulk metabolomics. By seamlessly integrating macroscopic organ-level imaging with microscopic spatial metabolomics, AVID establishes a new framework for spatial systems metabolism. Beyond myocardial infarction, this platform offers broad applicability to study organ-organ metabolic communication, spatial metabolic heterogeneity, and localized metabolic shifts across diverse physiological and pathological contexts, providing a transformative resource for metabolic research.
    Keywords:  ATP dynamics; CP: Metabolism; FRET; GO-ATeam biosensor; disease progression; energy metabolism; in vivo imaging; multiscale imaging; myocardial infarction; organ-organ interaction; spatial systems metabolism
    DOI:  https://doi.org/10.1016/j.celrep.2025.116246
  10. PLoS One. 2025 ;20(9): e0332065
      The mitochondrial oxidative phosphorylation (OXPHOS) system plays a pivotal role in the cell's energy conversion. The enzymes involved in OXPHOS are arranged in five protein-lipid complexes. The first four complexes (I-IV) form the mitochondrial respiratory chain, while Complex V is an F1Fo-ATP synthase. Mutations in genes involved in the biosynthesis of the OXPHOS complexes are an important cause of metabolic diseases. Blue-native polyacrylamide gel electrophoresis (BN-PAGE), originally developed by Hermann Schägger in the 1990s, has become instrumental in gaining insights into structure/function relationships of the OXPHOS system, including: (1) the assembly pathways of the complexes, (2) the composition of higher-order respiratory chain supercomplexes and (3) pathologic mechanisms in patients with a monogenetic OXPHOS disorder. We have used BN-PAGE for >20 years and validate here our recently published step-by-step laboratory protocol. This protocol describes the manual casting of native mini-gels and sample preparation for the resolution of individual OXPHOS complexes or respiratory chain supercomplexes. In addition to BN-PAGE, we explain the closely related clear-native (CN)-PAGE and two-dimensional BN/denaturing-PAGE techniques. Downstream applications include western blot analysis and in-gel enzyme activity staining for Complexes I, II, IV and V. Limitations of the technique are the comparative insensitivity of in-gel Complex IV activity staining and the lack of in-gel Complex III activity staining. Compared to other published BN-PAGE protocols, our protocol contains a shortened sample extraction procedure, advises when to use BN-PAGE and when to use CN-PAGE, and suggests a simple enhancement step for in-gel Complex V activity staining that markedly improves sensitivity. Our protocol is adaptable and yields robust, semi-quantitative and reproducible results.
    DOI:  https://doi.org/10.1371/journal.pone.0332065
  11. Sci Adv. 2025 Sep 19. 11(38): eadz9606
      Studies on the impact of metabolism on cell fate decisions are seeing a renaissance. However, a key challenge remains to distinguish signaling functions of metabolism from its canonical bioenergetic and biosynthetic roles, which underlie cellular homeostasis. Here, we tackled this challenge using mouse embryonic axis segmentation as an experimental model. First, we found that energetically subminimal amounts of glucose can support ongoing segmentation clock activity, providing evidence that glycolysis exerts a signaling function. Using a dynamical systems approach based on entrainment, we identified fructose 1,6-bisphosphate (FBP) as the potential signaling metabolite. Functionally, we demonstrated that glycolytic flux/FBP control the segmentation clock period and Wnt signaling in an anticorrelated manner. Critically, we showed that the slow segmentation clock phenotype caused by elevated glycolysis is mediated by Wnt signaling rather than cellular bioenergetic and biosynthetic state. Combined, our results demonstrate a modular organization of metabolic functions, revealing a signaling module of glycolysis that can be decoupled from its canonical metabolic functions.
    DOI:  https://doi.org/10.1126/sciadv.adz9606
  12. J Am Chem Soc. 2025 Sep 15.
      Arginine (Arg) is a critically important amino acid in the central nervous system and plays a pivotal role in the differentiation of neural stem cells (NSCs). However, specifically and quantitatively tracking Arg dynamics in situ presents a significant challenge. Herein, we developed a series of Arg probes (Rap1-9) based on the nucleophilic substitution reaction between a phenyl-activated ester and a primary amine. Among these, the optimized NIR-emission ratiometric fluorescent probe Rap-9 demonstrated the most pronounced electrophilicity at its reactive site, enabling rapid and specific detection of Arg both in vitro and in vivo. Notably, Rap-9 was successfully utilized for real-time imaging of Arg dynamics during O2·--stimulated NSC differentiation. Further studies revealed that Arg-mediated activation of the mTORC1 pathway could coordinate qNSC reactivation and neuronal differentiation by regulating mitochondrial energy metabolism from glycolysis to mitochondrial oxidative phosphorylation. These findings not only enhanced our understanding of the metabolic pathways governing NSC differentiation but also offered new perspectives for neuroscience research and potential therapeutic interventions.
    DOI:  https://doi.org/10.1021/jacs.5c05685
  13. bioRxiv. 2025 Sep 04. pii: 2025.08.30.673265. [Epub ahead of print]
      Certain forms of mitochondrial impairment confer longevity, while mitochondrial dysfunction arising from aging and disease-associated mutations triggers severe pathogenesis. The adaptive pathways that distinguish benefit from pathology remain unclear. Here we reveal that longevity induced by mitochondrial Complex I/ nuo-6 mutation in C. elegans is dependent on the endoplasmic reticulum (ER) Ca 2+ channel, InsP3R. We find that the InsP3R promotes mitochondrial respiration, but the mitochondrial calcium uniporter is dispensable for both respiration and lifespan extension in Complex I mutants, suggesting InsP3R action is independent of matrix Ca 2+ flux. Transcriptomic profiling and imaging reveal a previously unrecognized role for the InsP3R in regulating mitochondrial scaling, where InsP3R impairment results in maladaptive hyper-expansion of dysfunctional mitochondrial networks. We reveal a conserved InsP3R signaling axis through which calmodulin and actomyosin remodeling machineries, including Arp2/3, formin FHOD-1, and MLCK, constrain mitochondrial expansion and promote longevity. Disruption of actin remodeling or autophagy mimics InsP3R loss. Conversely, driving fragmentation ameliorates mitochondrial expansion and rescues longevity, supporting a model in which InsP3R-dependent actin remodeling sustains mitochondrial turnover. These findings establish an inter-organelle signaling axis by which ER calcium release orchestrates mitochondrial-based longevity through cytoskeletal effectors.
    DOI:  https://doi.org/10.1101/2025.08.30.673265
  14. Mol Cell. 2025 Sep 18. pii: S1097-2765(25)00706-3. [Epub ahead of print]85(18): 3486-3504.e7
      The mechanistic target of rapamycin (mTOR) is a key regulator of lipid homeostasis by controlling processes including lipid uptake and biosynthesis. mTOR dysregulation and consequent altered lipid metabolism are common in various diseases, including cancers, making mTOR a promising therapeutic target. Therefore, it is crucial to understand how mTOR activation and inhibition reprogram lipid homeostasis. In human cancer cell lines, mTOR inhibition induces alternative lipid uptake through translation eukaryotic initiation factor 3D (eIF3D)-mediated low-density lipoprotein receptor (LDLR)-related protein 6 (LRP6) increase and activates liver X receptor β (LXRβ), promoting cholesterol release from lysosomes and its transport to the plasma membrane via Niemann-Pick disease type C (NPC) intracellular cholesterol transporter 1 (NPC1). This signaling supports tumor cell survival and stress resistance. In mouse xenograft models, combining mTOR inhibition with LRP6 knockdown or NPC1 targeting significantly suppresses tumor growth. Our findings highlight mTOR feedback signaling in reprogramming lipid homeostasis and its therapeutic potential to treat diseases characterized by dysregulated mTOR.
    Keywords:  AKT; IGF1R; LRP6; NPC1; cholesterol; mTOR
    DOI:  https://doi.org/10.1016/j.molcel.2025.08.021
  15. Nature. 2025 Sep 17.
      The regulation of metabolic processes by proteins is fundamental to biology and yet is incompletely understood. Here we develop a mass spectrometry (MS)-based approach that leverages genetic diversity to nominate functional relationships between 285 metabolites and 11,868 proteins in living tissues. This method recapitulates protein-metabolite functional relationships mediated by direct physical interactions and local metabolic pathway regulation while nominating 3,542 previously undescribed relationships. With this foundation, we identify a mechanism of regulation over liver cysteine utilization and cholesterol handling, regulated by the poorly characterized protein LRRC58. We show that LRRC58 is the substrate adaptor of an E3 ubiquitin ligase that mediates proteasomal degradation of CDO1, the rate-limiting enzyme of the catabolic shunt of cysteine to taurine1. Cysteine abundance regulates LRRC58-mediated CDO1 degradation, and depletion of LRRC58 is sufficient to stabilize CDO1 to drive consumption of cysteine to produce taurine. Taurine has a central role in cholesterol handling, promoting its excretion from the liver2, and we show that depletion of LRRC58 in hepatocytes increases cysteine flux to taurine and lowers hepatic cholesterol in mice. Uncovering the mechanism of LRRC58 control over cysteine catabolism exemplifies the utility of covariation MS to identify modes of protein regulation of metabolic processes.
    DOI:  https://doi.org/10.1038/s41586-025-09535-5
  16. bioRxiv. 2025 Sep 08. pii: 2025.09.04.674092. [Epub ahead of print]
      CNS has an overall higher level of lipids than all tissues except adipose and contains up to 25% of total body cholesterol. Recent data demonstrate a complex crosstalk between lipid metabolism and inflammation, suggesting potential contribution of the lipid-rich brain environment to neuroinflammation. While recent data support the importance of brain lipid environment to inflammatory changes observed in age related chronic neurodegenerative diseases, in vivo interactions between lipid environment, lipid metabolism and neuroinflammation in acute brain disease and injury remain poorly understood. Here we utilize a mouse model of traumatic brain injury (TBI) to demonstrate that acute neurotrauma leads to widespread lipid metabolism reprograming in all microglial and brain associated and infiltrating monocyte populations. Additionally, we identify unique microglial and monocyte populations with higher degree of lipid metabolism reprograming and pronounced accumulation of neutral storage lipids, including cholesteryl esters and triglycerides. These lipids accumulate not only in lipid droplets but also in the microglial and monocyte lysosomes and are associated with lysosomal dysfunction and inhibition of autophagy after TBI. Our data indicate that lipid accumulation in these cells is the result of altered lipid handling rather than lipid synthesis and is triggered by phagocytosis of lipid-rich myelin debris generated after TBI. Finally, we use mice with autophagy defects in microglia and monocytes to demonstrate that further inhibition of autophagy leads to more pronounced lipid metabolism reprograming and exacerbated cellular lipid accumulation. Our data suggest a pathological feedback loop, where lipid phagocytosis causes inhibition of autophagy-lysosomal function, which in turn exacerbates cellular lipid retention, reprograming and inflammation.
    DOI:  https://doi.org/10.1101/2025.09.04.674092
  17. ACS Med Chem Lett. 2025 Sep 11. 16(9): 1814-1824
      A novel nucleoside analogue, LCB-2151, has been developed to induce cell death in KRAS-mutated pancreatic human cancer cell lines, which exhibit partial resistance to gemcitabine, a widely used anticancer drug. LCB-2151 disrupts the two primary sources of ATP production, namely, glycolysis and mitochondrial oxidative phosphorylation, reducing the bioenergetic capacity of these cells and inducing the formation of reactive oxygen species. Metabolomics and mitochondrial respiration analyses reveal that LCB-2151 inhibits key enzymes in glycolysis, the TCA cycle, and fatty acid β-oxidation. These findings highlight a coordinated mechanism driving bioenergetic disruption and cell death.
    Keywords:  KRAS; Pancreatic ductal adenocarcinoma; nucleoside analogues; stereogenic all-carbon quaternary center
    DOI:  https://doi.org/10.1021/acsmedchemlett.5c00378
  18. Biol Chem. 2025 Sep 15.
      Mitochondria are essential for cellular metabolism, serving as the primary source of adenosine triphosphate (ATP). This energy is generated by the oxidative phosphorylation (OXPHOS) system located in the inner mitochondrial membrane. Impairments in this machinery are linked to serious human diseases, especially in tissues with high energy demands. Assembly of the OXPHOS system requires the coordinated expression of genes encoded by both the nuclear and mitochondrial genomes. The mitochondrial DNA encodes for 13 protein components, which are synthesized by mitochondrial ribosomes and inserted into the inner membrane during translation. Despite progress, key aspects of how mitochondrial gene expression is regulated remain elusive, largely due to the organelle's limited genetic accessibility. However, emerging technologies now offer new tools to manipulate various stages of this process. In this review, we explore recent strategies that expand our ability to target mitochondria genetically.
    Keywords:  RNA; gene expression; genetic tools; mitochondria
    DOI:  https://doi.org/10.1515/hsz-2025-0170
  19. J Cell Sci. 2025 Sep 17. pii: jcs.263983. [Epub ahead of print]
      Astrocytes degrade fatty acids in response to glutamate while reducing the abundance of lipid droplets. But how glutamate regulates lipid droplets in astrocytes is unclear. Here we show that glutamate decreases the amount of reactive oxygen species which in turn, reduces autophagy and the amount of lipids in need of storage in lipid droplets. This decrease in lipid droplets and reactive oxygen species occurs independent of glutamate import through excitatory amino acid transporters (EAATs). However, activation of AMPK, downstream of EAATs, further promotes a decrease in lipid droplets. Glutamate also increases the pool of fused mitochondria capable of maintaining enhanced fatty acid metabolism. Our work reveals how astrocytic metabolism is regulated by glutamate that can serve to coordinate astrocyte physiology with neuronal activity.
    Keywords:  Astrocytes; Autophagy; Fatty acid oxidation; Lipid droplet; Lipid peroxidation; Oxidative stress
    DOI:  https://doi.org/10.1242/jcs.263983
  20. Neurophotonics. 2025 Jun;12(Suppl 2): S22806
      Understanding molecular transport in the brain in vivo is essential for elucidating how the brain regulates its metabolism, how neurological pathologies develop, and why many brain-targeted drugs fail. Two-photon microscopy (TPM) is the gold standard for in vivo imaging in highly scattering tissues such as the brain. However, suboptimal use of TPM can compromise study outcomes due to the inherent challenges of in vivo imaging. We highlight the importance of optimizing both spatial and temporal resolution in TPM to ensure accurate data acquisition and interpretation. We compare TPM-based studies of molecular transport with traditional wide-field microscopy approaches, emphasizing how light scattering in brain tissue limits the effectiveness of the latter. We discuss the impact of motion blur-arising from diffusion of tracers or natural movement of cerebral vasculature-on image quality and offer practical strategies to mitigate these effects. In addition, we address the complexities of statistically analyzing noisy images, typically occurring due to low-photon budgets or the need for fast image recording in in vivo TPM. We conclude with a set of practical guidelines for effective data acquisition, aimed at facilitating the implementation of the concepts discussed. When properly optimized, TPM is a powerful tool capable of revealing fundamental mechanisms of brain transport and advancing our understanding of cerebral metabolism.
    Keywords:  brain; diffusion; motion blur; resolution; transport; two-photon microscopy
    DOI:  https://doi.org/10.1117/1.NPh.12.S2.S22806
  21. Chem Sci. 2025 Sep 05.
      Predicting drug metabolism remains a long-standing challenge in pharmacokinetics due to the mechanistic complexity of enzymatic transformations and the fragmented nature of current computational tools. Existing models are typically limited to isolated tasks - substrate recognition, metabolic site identification, or metabolite generation - lacking mechanistic fidelity, holistic integration, and chemical interpretability. Here, we introduce DeepMetab, the first comprehensive and mechanistically informed deep graph learning framework for end-to-end prediction of CYP450-mediated drug metabolism. DeepMetab uniquely integrates three essential prediction tasks - substrate profiling, site-of-metabolism (SOM) localization, and metabolite generation - within a unified multi-task architecture. It employs a dual-labeling strategy that simultaneously captures atom- and bond-level reactivity, and infuses multi-scale features including quantum-informed and topological descriptors into a graph neural network (GNN) backbone. A curated knowledge base of expert-derived reaction rules further ensures mechanistic consistency during metabolite synthesis. DeepMetab consistently outperformed existing models across nine major CYP isoforms in all three prediction tasks. Its strong generalizability was further validated on 18 recently FDA-approved drugs, achieving 100% TOP-2 accuracy for SOM prediction and accurately recovering several experimentally confirmed metabolites absent from the training set. Visualization of learned representations reveals expert-level discernment of electronic characteristics, steric architecture, and regiochemical determinants, underscoring the model's interpretability. Together, DeepMetab represents a next-generation AI system that bridges symbolic reaction rules and deep graph reasoning to deliver accurate, interpretable, and end-to-end metabolism predictions, offering tangible value for both preclinical research and regulatory applications.
    DOI:  https://doi.org/10.1039/d5sc04631a
  22. Biochim Biophys Acta Rev Cancer. 2025 Sep 16. pii: S0304-419X(25)00195-7. [Epub ahead of print] 189453
      The process of mitochondrial fission is a major determinant of mitochondrial homeostasis. DRP1 is the chief architect of the mitochondrial fission process, and the DRP1 recruitment to the mitochondrial outer membrane is necessary for the mitochondrial division. DRP1 contributes to cancer progression by promoting cell proliferation, enhancing resistance to therapy, inhibiting mitochondrial-mediated apoptosis, suppressing immune responses, and sustaining cancer stem cell heterogeneity and self-renewal. Moreover, DRP1 drives metabolic reprogramming to support enhanced energy production and biosynthesis required for tumor growth and survival. In addition, DRP1-mediated mitochondrial fission also favours NLRP3 inflammasome activation within the tumor microenvironment, which regulates cancer progression. Interestingly, elevated levels of DRP1 expression have been identified as a significant prognostic marker, correlating with poor survival outcomes across multiple cancer types. Many DRP1 inhibitors have been developed for cancer treatment, but more specific and selective agents are needed to improve efficacy and reduce off-target effects. A comprehensive understanding of DRP1's role in cancer cells is essential for developing DRP1 inhibitors, which hold promise as novel anticancer therapies and may enhance the effectiveness of conventional treatments.
    Keywords:  Cancer; Chemoresistance; DRP1; Metabolic reprograming; Mitochondrial fission; NLRP3 inflammasome
    DOI:  https://doi.org/10.1016/j.bbcan.2025.189453
  23. Proc Natl Acad Sci U S A. 2025 Sep 23. 122(38): e2505752122
      Kidney fibrosis is driven by multiple factors, among which impaired fatty acid oxidation has emerged as a critical determinant. Acyl-Coenzyme A (CoA) synthetase medium-chain family member 3 (ACSM3), a key enzyme of medium-chain fatty acid (MCFA) metabolism, has been implicated in metabolic syndrome, but its function in fibrotic kidney remains unexplored. Here, we found that tubular epithelial ACSM3 expression was downregulated in kidney fibrotic mice and patients and inversely correlated with disease severity. Systemic and tubular-specific knockout of ACSM3 both exacerbated renal fibrosis, whereas adeno-associated virus (AAV)-mediated ACSM3 overexpression alleviated fibrotic kidneys in mice. Mechanistically, ACSM3 deficiency disrupted MCFA metabolism and resulted in abnormal mitochondrial homeostasis. Notably, we identified that dodecanoic acid (C12:0) could improve kidney fibrosis, which was primarily utilized via ACSM3 in kidneys. Furthermore, C12:0 oxidation impairment caused by tubular ACSM3 deficiency aggravated fibrotic kidney. Together, ACSM3-regulated MCFA metabolism played a pivotal role in kidney fibrosis, highlighting a potent drug target of ACSM3 and a potential supplementary therapy of MCFA against chronic kidney disease.
    Keywords:  ACSM3; fatty acid oxidation; kidney fibrosis; medium-chain fatty acids
    DOI:  https://doi.org/10.1073/pnas.2505752122
  24. bioRxiv. 2025 Sep 09. pii: 2025.06.09.658730. [Epub ahead of print]
      Proper heme biosynthesis is essential for numerous cellular functions across nearly all life forms. In humans, dysregulated heme metabolism is linked to multiple blood diseases, neurodegeneration, cardiovascular disease, and metabolic disorders. Erythroid heme production begins with the rate-limiting enzyme Aminolevulinic Acid Synthase (ALAS2) in the mitochondrion. Although prior studies discuss the regulation of ALAS2 in the nucleus and cytoplasm, its modulation as a mature mitochondrial matrix enzyme remains poorly understood. We report that heme binds mature human ALAS2 with high affinity, acting as a reversible mixed inhibitor that reduces enzymatic activity. Structure-based modeling reveals two flexible regions of ALAS2 interact with heme, locking the enzyme in an inactive conformation and occluding the active site. Our work reveals a negative feedback mechanism for heme synthesis, offering insights into the spatial regulation of ALAS2 and the maturation of the essential heme cofactor.
    DOI:  https://doi.org/10.1101/2025.06.09.658730
  25. Nature. 2025 Sep 17.
      Brown and beige adipocytes express uncoupling protein 1 (UCP1), a mitochondrial protein that dissociates respiration from ATP synthesis and promotes heat production and energy expenditure. However, UCP1-/- mice are not obese1-5, consistent with the existence of alternative mechanisms of thermogenesis6-8. Here we describe a UCP1-independent mechanism of thermogenesis involving ATP-consuming metabolism of monomethyl branched-chain fatty acids (mmBCFA) in peroxisomes. These fatty acids are synthesized by fatty acid synthase using precursors derived from catabolism of branched-chain amino acids9 and our results indicate that β-oxidation of mmBCFAs is mediated by the peroxisomal protein acyl-CoA oxidase 2 (ACOX2). Notably, cold exposure upregulated proteins involved in both biosynthesis and β-oxidation of mmBCFA in thermogenic fat. Acute thermogenic stimuli promoted translocation of fatty acid synthase to peroxisomes. Brown-adipose-tissue-specific fatty acid synthase knockout decreased cold tolerance. Adipose-specific ACOX2 knockout also impaired cold tolerance and promoted diet-induced obesity and insulin resistance. Conversely, ACOX2 overexpression in adipose tissue enhanced thermogenesis independently of UCP1 and improved metabolic homeostasis. Using a peroxisome-localized temperature sensor named Pexo-TEMP, we found that ACOX2-mediated fatty acid β-oxidation raised intracellular temperature in brown adipocytes. These results identify a previously unrecognized role for peroxisomes in adipose tissue thermogenesis characterized by an mmBCFA synthesis and catabolism cycle.
    DOI:  https://doi.org/10.1038/s41586-025-09517-7
  26. Trends Endocrinol Metab. 2025 Sep 12. pii: S1043-2760(25)00174-2. [Epub ahead of print]
      Type 2 diabetes (T2D) manifests as profound systemic metabolic dysregulation. Mounting evidence indicates T2D significantly impairs T cell immunity, compromising both protective immune responses and immune homeostasis. This dysfunction stems from the multitude roles of metabolites in T cell biology: energy substrates, signaling molecules, and epigenetic regulators. In this review, we synthesize current evidence on how the metabolic hallmarks of T2D (hyperglycemia, hyperinsulinemia, and dyslipidemia) reprogram T cell metabolism and their functionalities. Notably, most patients with T2D receive combination antidiabetic therapies which not only correct systemic metabolism but also exert direct immunomodulatory effects on T cells. Unraveling the interplay between disease-driven metabolic perturbations and pharmacologically induced immunomodulation is essential to advance therapeutic strategies that restore immune competence while preserving immunoregulatory balance.
    Keywords:  T cells; immunometabolism; type 2 diabetes
    DOI:  https://doi.org/10.1016/j.tem.2025.08.005