bims-celmim Biomed News
on Cellular and mitochondrial metabolism
Issue of 2026–01–11
seventeen papers selected by
Marc Segarra Mondejar, AINA



  1. bioRxiv. 2025 Dec 30. pii: 2025.12.30.693754. [Epub ahead of print]
      Mitochondria are dynamic organelles that can fragment or fuse to support different bioenergetic demands (e.g., glycolysis vs. oxidative phosphorylation) and distinct cell behaviors (e.g., mitosis or migration). While the role of mitochondrial dynamics in wound healing and metabolic disorders has received significant attention, the role of mitochondrial fission and fusion during normal embryonic development is less well understood--in part due to the difficulty of studying such processes in vivo . Combined with the depth-resolved imaging capabilities of multiphoton microscopy, fluorescence lifetime imaging (FLIM) of the mitochondrial cofactor NADH can be used to simultaneously visualize mitochondrial network morphology and infer certain aspects of cellular bioenergetics (e.g., glycolysis vs. oxidative phosphorylation) in a label-free, non-invasive manner. Here we demonstrate that NADH FLIM can be used to accurately track the subcellular localization and topology of mitochondrial networks in live Drosophila embryos. We used this technique to assess whether cells show changes in NADH lifetime during convergent extension (CE)--a conserved process of tissue remodeling in which thousands of germband cells undergo coordinated intercalation to drive elongation of the head-to-tail axis. Contrary to our expectations, we did not observe significant changes in NADH lifetime or network appearance during CE in wild-type embryos, suggesting that germband cells do not need to alter their baseline metabolism to fuel cell intercalation during normal development. To directly assess the role of mitochondrial fission and fusion during CE, we used RNA interference to disrupt the fission mediator Drp1 and the fusion mediator Opa1 . Consistent with expectations, inhibiting mitochondrial fission in Drp1- knockdown embryos led to hyper-fused networks and significantly longer NADH lifetimes, indicating a shift towards oxidative phosphorylation. Conversely, inhibiting mitochondrial fusion in Opa1- knockdown embryos led to more hyper-fragmented networks and significantly shorter NADH lifetimes, indicating a shift towards glycolysis. Interestingly, inhibiting either fission or fusion altered tissue elongation and greatly increased the rate of cell intercalation errors, suggesting that a precise network topology is required for proper CE. We hypothesize that the CE defects in Drp1 -knockdown embryos are primarily due to incorrect basal subcellular localization of mitochondria, whereas the CE defects in Opa1 -knockdown embryos are due to deficient ATP and/or ROS production. These experiments demonstrate the utility of FLIM-based applications for characterizing the role of mitochondria during normal embryonic development, which could yield a better understanding of the metabolic underpinnings of various pathologies that involve epithelial remodeling, including spina bifida, defective wound healing, and cancer metastasis.
    DOI:  https://doi.org/10.64898/2025.12.30.693754
  2. EMBO Rep. 2026 Jan 03.
      Astrocytes, the most abundant glial cell type in the central nervous system, have traditionally been viewed from the perspective of metabolic support, particularly supplying neurons with lactate via glycolysis. This view has focused heavily on glucose metabolism as the primary mode of sustaining neuronal function. However, recent research challenges this paradigm by positioning astrocytes as dynamic metabolic hubs that actively engage in lipid metabolism, especially mitochondrial fatty acid β-oxidation. Far from serving solely as an energy source, fatty acid ß-oxidation in astrocytes orchestrates reactive oxygen species-mediated signaling pathways that modulate neuron-glia communication and cognitive outcomes. This review integrates recent advances on astrocytic fatty acid ß-oxidation and ketogenesis, alongside other metabolic pathways converging on reactive oxygen species dynamics, including cholesterol metabolism and peroxisomal β-oxidation. In reframing astrocytic metabolism from energy provision to signaling, we propose new directions for understanding central nervous system function and dysfunction.
    Keywords:  Astrocytes; Fatty Acid β-Oxidation; Ketogenesis; Neuron-glia Metabolic Coupling; Reactive Oxygen Species Signaling
    DOI:  https://doi.org/10.1038/s44319-025-00683-3
  3. Mol Metab. 2026 Jan 06. pii: S2212-8778(25)00223-6. [Epub ahead of print] 102316
      Following recurrence, the cornerstone clinical therapy to treat prostate cancer (PCa) is to inhibit the androgen receptor (AR) signaling. While AR inhibition is initially successful, tumors will eventually develop treatment resistance and evolve into lethal castration-resistant PCa. To discover new anti-metabolic treatments for PCa, a high-throughput anti-metabolic drug screening was performed in PC3 cells, an AR-negative PCa cell line. This screening identified the dihydroorotate dehydrogenase (DHODH) enzyme as a metabolic vulnerability, using both AR-positive and AR-negative models, including the neuroendocrine cell line LASCPC-01 and patient-derived organoids. DHODH is required for de novo pyrimidine synthesis and is the sole mitochondrial enzyme of this pathway. Using extracellular flux assays and targeted metabolomics, DHODH inhibition was shown to impair the pyrimidine synthesis pathway, as expected, along with a significant reprogramming of mitochondrial metabolism, with a massive increase in fumarate (>10-fold). Using 13C6-glucose, it was shown that following DHODH inhibition, PCa cells redirect carbons from glucose toward biosynthetic pathways rather than the TCA cycle. In parallel, using 13C5-glutamine, it was shown that PCa cells use this amino acid to fuel a reverse TCA cycle. Finally, 13C1-aspartate and 15N1-glutamine highlighted the connection between pyrimidine synthesis and the urea cycle, redirecting pyrimidine synthesis intermediates toward the urea cycle as a stress response mechanism upon DHODH inhibition. Consequently, combination therapies targeting DHODH and glutamine metabolism were synergistic in impairing PCa cell proliferation. Altogether, these results highlight DHODH as a metabolic vulnerability of AR-positive and AR-negative PCa cells by regulating central carbon and nitrogen metabolism.
    Keywords:  BAY-2402234; DHODH; NEPC; androgen receptor; aspartate; cancer metabolism; castration-resistant prostate cancer; glucose; glutamine; mitochondria; neuroendocrine differentiation; neuroendocrine prostate cancer; nucleotide synthesis; prostate cancer
    DOI:  https://doi.org/10.1016/j.molmet.2025.102316
  4. Mol Cell. 2026 Jan 08. pii: S1097-2765(25)01013-5. [Epub ahead of print]86(1): 6-8
      In this issue of Molecular Cell, Zhu et al.1 show that mitochondria of cancer cells rely on the import of glutamine not only to fuel metabolite synthesis via the tricarboxylic acid cycle but also to charge mt-tRNAGln to allow mitochondrial protein synthesis and respiration.
    DOI:  https://doi.org/10.1016/j.molcel.2025.12.014
  5. PLoS Biol. 2026 Jan;24(1): e3003570
      Metabolic rewiring of immune cells has broad impacts on immune responses and disease outcomes. Systems biology approaches, such as multi-omics profiling and perturbation screening, could uncover new actionable targets and therapeutic avenues to explore.
    DOI:  https://doi.org/10.1371/journal.pbio.3003570
  6. Glia. 2026 Mar;74(3): e70131
      Microglia, the brain's innate immune cells, possess complex, highly motile branched processes. These act independently, enabling individual processes to carry out entirely distinct functions in parallel. Intracellular Ca2+ signaling is implicated in many of these distinct microglial functions. However, it has been difficult to quantify how such Ca2+ activity is compartmentalized in space and time to prevent unwanted cross-talk between signaling pathways. Previous studies have typically relied on manually drawn regions-of-interest (ROIs), which averages fluorescence within predefined compartments and therefore cannot resolve the fine-scale spatio-temporal propagation patterns that may be functionally relevant. To address this, we adopt an unbiased non-ROI-based analytical approach to comprehensively characterize the temporal, spatial and spatio-temporal dimensions of microglial Ca2+ activity in vivo. We find that microglial Ca2+ activity predominantly occurs in processes, tends to remain localized at its site of origin, and, when it propagates, often follows a well-defined direction (either toward or away from the soma) rather than spreading isotropically as would be expected under purely passive diffusion. The tendency of microglial Ca2+ activity to spread between intracellular regions does not correlate with peak amplitude, but appears to be limited by the branching points of the microglial processes. Finally, we show that Ca2+ activity can differ between the microglial soma and its processes in response to various pharmacological stimuli. These results suggest that Ca2+ signals are actively compartmentalized within microglia in a context dependent manner, rather than being synchronized across the entire cell.
    Keywords:   P2Y12 ; Ca2+ imaging; awake state; in vivo two‐photon imaging; microglia; neuronal activity; purinergic signaling
    DOI:  https://doi.org/10.1002/glia.70131
  7. Mol Cell. 2026 Jan 08. pii: S1097-2765(25)00980-3. [Epub ahead of print]86(1): 135-149.e9
      Mitochondria and the endoplasmic reticulum (ER) contain large areas that are in close proximity. Yet the mechanism of how these inter-organellar adhesions are formed remains elusive. Tight functional connections, termed "membrane contact sites," assemble at these areas and are essential for exchanging metabolites and lipids between the organelles. Recently, the ER-resident protein PDZ domain-containing protein 8 (PDZD8) was identified as a tether between the ER and mitochondria or late endosomes/lysosomes. Here, we show that PDZD8 can undergo phase separation via its intrinsically disordered region (IDR). Endogenously labeled PDZD8 forms condensates on membranes both in vitro and in mammalian cells. Electron microscopy analyses indicate that the expression of full-length PDZD8 rescues the decrease in inter-organelle contacts in PDZD8 knockout cells but not PDZD8 lacking its IDR. Together, this study identifies that PDZD8 condensates at the lipid interfaces act as an adhesive framework that stitches together the neighboring organelles and supports the structural and functional integrity of inter-organelle communication.
    Keywords:  PDZD8; biomolecular condensates; endoplasmic reticulum; liquid-liquid phase separation; membrane contact sites; mitochondria
    DOI:  https://doi.org/10.1016/j.molcel.2025.12.006
  8. Nat Cell Biol. 2026 Jan 07.
      Changes in cell state are often accompanied by altered metabolic demands, and homeostasis depends on cells adapting to their changing needs. One major cell state change is senescence, which is associated with dramatic changes in cell metabolism, including increases in lipid metabolism, but how cells accommodate such alterations is poorly understood. Here we show that the transcription factor p53 increases recycling of the lipid headgroups required to meet the increased demand for membrane phospholipids during senescence. p53 activation increases the supply of phosphoethanolamine, an intermediate in the Kennedy pathway for de novo synthesis of phosphatidylethanolamine, in part by increasing lipid turnover and transactivating genes involved in autophagy and lysosomal catabolism that enable membrane turnover. Disruption of phosphoethanolamine conversion to phosphatidylethanolamine is well tolerated in the absence of p53 but results in dramatic organelle remodelling and perturbs growth and gene expression following p53 activation. Consistently, CRISPR-Cas9-based genetic screens reveal that p53-activated cells preferentially depend on genes involved in lipid metabolism and lysosomal function. Together, these results reveal lipid headgroup recycling to be a homeostatic function of p53 that confers a cell-state-specific metabolic vulnerability.
    DOI:  https://doi.org/10.1038/s41556-025-01853-0
  9. Cell Res. 2026 Jan;36(1): 11-37
      Mitophagy, an evolutionarily conserved quality-control process, selectively removes damaged mitochondria to maintain cellular homeostasis. Recent advances in our understanding of the molecular machinery underlying mitophagy - from receptors and stress-responsive triggers to lysosomal degradation - illustrate its key role in maintaining mitochondrial integrity and adapting mitochondrial function to ever-changing physiological demands. In this review, we outline the fundamental mechanisms of mitophagy and discuss how dysregulation of this pathway disrupts mitochondrial function and metabolic balance, driving a wide range of disorders, including neurodegenerative, cardiovascular, metabolic, and immune-related diseases, as well as cancer. We explore the dual role of mitophagy as both a disease driver and a therapeutic target, highlighting the efforts and challenges of translating mechanistic insights into precision therapies. Targeting mitophagy to restore mitochondrial homeostasis may be at the center of a large range of translational opportunities for improving human health.
    DOI:  https://doi.org/10.1038/s41422-025-01203-7
  10. Biochim Biophys Acta Rev Cancer. 2026 Jan 06. pii: S0304-419X(26)00002-8. [Epub ahead of print] 189530
      Metabolic reprogramming, exemplified by the Warburg effect, is a hallmark of cancer. Hexokinase 2 (HK2), a key glycolytic enzyme, is frequently overexpressed in cancer, sustaining glucose metabolism and tumor progression. MicroRNAs (miRNAs) post-transcriptionally regulate HK2 by targeting its 3'untranslated region or upstream signaling pathways. While monotherapies often fail due to compensatory pathways and drug resistance, dual-targeting both HK2 and its regulatory miRNAs could achieve substantial metabolic inhibition. This review summarizes recent advances in miRNA-HK2 regulatory networks across cancers and highlights dual-targeting miRNA-HK2 as a promising therapeutic strategy to overcome metabolic plasticity and improve precision, durability, and efficacy in cancer therapy.
    Keywords:  Cancer therapy; Dual-targeting; Hexokinase 2; Metabolic reprogramming; MicroRNAs
    DOI:  https://doi.org/10.1016/j.bbcan.2026.189530
  11. Science. 2026 Jan 08. eady5532
      Environmental adaptation often involves a shift in energy utilization toward mitochondrial fatty acid oxidation, which requires carnitine. Besides dietary sources of animal origin, carnitine biosynthesis from trimethyllysine (TML) is essential, particularly for those who consume plant-based diets; however, its molecular regulation and physiological role remain elusive. Here, we identify SLC25A45 as a mitochondrial TML carrier that controls carnitine biosynthesis and fuel switching. SLC25A45 deficiency decreased the carnitine pool and impaired mitochondrial fatty acid oxidation, shifting reliance to carbohydrate metabolism. Slc25a45-deficient mice were cold-intolerant and resistant to lipid mobilization by GLP1 receptor agonist (GLP-1RA), rendering them resistant to adipose tissue loss. Our study suggests that mitochondria serve as a regulatory checkpoint in fuel switching, with implications for metabolic adaptation and the efficacy of GLP-1RA-based anti-obesity therapy.
    DOI:  https://doi.org/10.1126/science.ady5532
  12. Glia. 2026 Mar;74(3): e70136
      Astrocytes are central to lipid metabolism in the central nervous system. Due to their morphological and functional characteristics, astrocytes can uptake fatty acids (FAs) from the bloodstream and extracellular space and store them in lipid droplets (LD). LD are dynamic organelles, whose accumulation in astrocytes has been shown to occur upon exposure to various stress stimuli. Different hypotheses proposed to explain motor neuron degeneration in amyotrophic lateral sclerosis (ALS) implicate mitochondrial dysfunction and oxidative stress. Mitochondrial dysfunction in astrocytes is associated with elevation of cytoplasmic lipids and lipid-binding proteins. We observed increased LD in the spinal cord of symptomatic ALS mice, as well as in human transdifferentiated astrocytes obtained from ALS patients. Using a co-culture model, we examined the effect of FA overload and its impact on astrocyte-motor neuron interaction. LD accumulation was tightly coupled with an NF-κB-driven proinflammatory response in nontransgenic astrocytes, correlating with motor neuron toxicity. These results provide additional evidence to the notion that altered energy balance may contribute to neuronal death in ALS. Furthermore, pharmacological inhibition of lactate dehydrogenase (LDH) reversed LD accumulation in mouse and human astrocytes expressing ALS-linked mutations. Genetic ablation of LDHA similarly reduced LD accumulation in response to FA treatment. Collectively, our data underscore the role of lipid metabolism in astrocyte-neuron interactions in ALS models and suggest that LD accumulation, rather than serving solely as a protective mechanism, reflects a metabolic stress state linked to a detrimental phenotypic transformation in astrocytes.
    Keywords:  LDH; NF‐κB; astrocytes; inflammation; lipid droplets
    DOI:  https://doi.org/10.1002/glia.70136
  13. FASEB J. 2026 Jan 15. 40(1): e71421
      Acute kidney injury (AKI) is a global health concern with various etiologies, including ischemia-reperfusion injury, sepsis, and nephrotoxic agents such as cisplatin. Cisplatin-induced nephrotoxicity is associated with lysosomal damage, but the underlying mechanisms remain unclear. This study aimed to elucidate the role of lysosomal damage in cisplatin-induced cell death in tubular epithelial cells (TECs). AKI models were induced using cisplatin both in vivo and in vitro. Mouse kidney morphology and function were assessed using biochemical assays, immunohistochemistry, and histological staining techniques such as HE, PAS, and TUNEL. RNA sequencing analysis and pharmacological interventions were used to investigate the specific mechanism in cisplatin-induced TECs injury. The distribution and expression of lysosomes and calcium (Ca2+) were measured through immunofluorescence staining, Western blotting, and confocal microscopy. RNA sequencing analysis revealed a notable role of Ca2+ signaling pathways in cisplatin-induced nephrotoxicity. We demonstrated that cisplatin exposure induced significant lysosomal abnormalities, including altered distribution, morphology, and increased Ca2+ leakage. This dysregulation of lysosomal Ca2+ homeostasis was closely correlated with TECs apoptosis. Mechanistically, we show that lysosome Ca2+ release activates calcineurin, thereby triggering apoptosis in TECs. Preliminary data indicate that inhibiting lysosomal Ca2+ release through targeting TRPML1 may mitigate cisplatin-induced AKI. Our study reveals a lysosomal Ca2+-calcineurin pathway that contributes to cisplatin-induced nephrotoxicity and offers potential therapeutic targets.
    Keywords:  TRPML1; apoptosis; calcineurin; cisplatin‐induced AKI; lysosomal Ca2+ homeostasis
    DOI:  https://doi.org/10.1096/fj.202501365RRR
  14. Nat Commun. 2026 Jan 08.
      Healthy mitochondria are crucial for maintaining neuronal homeostasis. Their activity depends on a dynamic lipid and protein exchange through fusion, fission, and vesicular trafficking. Studying vesicles in neurons is challenging with conventional microscopy due to their small size, heterogeneity, and dynamics. We use multicolour stimulated emission depletion nanoscopy to uncover the ultrastructure of mitochondrial-derived vesicles (MDVs) in live neurons, biosensors to define their functional state, and a pulse-chase strategy to identify their turnover in situ. We identified three populations of vesicular structures: one transporting degradation products originating from oxidative stress, one shuttling cargo and newly translated proteins for local organelle biogenesis and one consisting of small, functional mitochondria. Furthermore, we provide evidence supporting that de novo peroxisomes biogenesis occurs via the fusion of endoplasmic reticulum and MDVs at mitochondrial sites. Our data provide mechanistic insight into organelle biogenesis driven by significant diversity in MDV morphology, functional state, and molecular composition.
    DOI:  https://doi.org/10.1038/s41467-025-68160-y
  15. PLoS One. 2026 ;21(1): e0339326
      Mitochondrial bioenergetics are vital for ATP production and are associated with several diseases, including Parkinson's Disease (PD). Here, we simulated a computational model of mitochondrial ATP production to interrogate mitochondrial bioenergetics under physiological and pathophysiological conditions, and provide a data resource that can be used to interpret mitochondrial bioenergetics experiments. We first characterised the impact of several common electron transport chain (ETC) impairments on experimentally-observable bioenergetic parameters. We then established an analysis pipeline to integrate simulations with experimental data and predict the molecular defects underlying experimental bioenergetic phenotypes. We applied the pipeline to data from PD models. We verified that the impaired bioenergetic profile previously measured in Parkin knockout (KO) neurons can be explained by increased mitochondrial uncoupling. We then generated primary cortical neurons from a Pink1 KO mouse model of PD, and measured reduced oxygen consumption rate (OCR) capacity and increased resistance to Complex III inhibition. Here, our pipeline predicted that multiple impairments are required to explain this bioenergetic phenotype. Finally, we provide all simulated data as a user-friendly resource that can be used to interpret mitochondrial bioenergetics experiments, predict underlying molecular defects, and inform experimental design.
    DOI:  https://doi.org/10.1371/journal.pone.0339326
  16. bioRxiv. 2025 Dec 31. pii: 2025.12.30.697119. [Epub ahead of print]
      Cell mechanics play significant roles in all aspects of cell function. While many types of fluorescent linear force sensors inserted in cellular fibrillar elements have been developed, few tools are available to track two-dimensional tension in cell membranes. Here, we present a novel principle for tension detection using a fluorescent probe based on the scaffold of the GsMTx4 peptide from Grammostola venom. Previously, we have shown that amphipathic GsMTx4 binds to lipids and inhibits mechanosensitive channels by inserting more deeply into the membrane at tensions near activation thresholds, thereby acting as a buffer clamping lateral pressure in the bilayer. We leverage this property of GsMTx4 to redistribute between the 'shallow' and 'deep' immersion states, thereby designing probes with a fluorescent moiety that increases quantum yield in nonpolar environments. GsMTx4 analogs carrying fluorescent groups at the two positions increase fluorescence intensity in osmotically shocked liposomes and aspirated giant vesicles in a near-linear fashion in response to physiological bilayer tensions. The responses show dependence on membrane composition, particularly lipid charge and the presence of lipid-ordering components, such as sphingomyelin and cholesterol. Langmuir compression isotherms recorded in the presence of NBD analogs indicated initial incorporation into the monolayer, followed by sharp expulsion at the monolayer-bilayer equivalence pressure, with correlated changes in monolayer compressibility and fluorescence, illustrating the basic principle of probe action. The probes show promise for monitoring tension in biological membranes at low, non-inhibitory concentrations. Experiments with native cell-derived membrane vesicles reveal heterogeneous baseline staining and tension responses, underscoring the probes' selectivity for distinct membrane domains.
    Significance: Cell mechanics are crucial for all cell functions, including division, survival, migration, and differentiation. Although many versions of fluorescent linear force sensors have been developed for cytoskeletal and ECM elements, few tools exist to monitor two-dimensional tension in cell membranes. Many cells are motile, actively deforming their membrane, supported and driven by the underlying cytoskeleton. There is a two-order-of-magnitude discrepancy between membrane tension estimates from the tether formation technique and the tensions that activate common mechanosensitive channels in most cells. This discrepancy highlights the need for non-invasive membrane probes that can independently measure membrane tension, especially since it can be highly localized and dynamic. Here, we introduce such probes and a new principle for tension measurement.
    DOI:  https://doi.org/10.64898/2025.12.30.697119
  17. Neuron. 2026 Jan 07. pii: S0896-6273(25)00929-8. [Epub ahead of print]114(1): 4-5
      In this issue of Neuron, Li et al.1 show that follistatin-like 1 (FSTL1) emerges as a critical hypothalamic insulin sensitizer, whose pharmacological targeting attenuates body weight gain and improves systemic glucose metabolism, highlighting brain insulin signaling amplification as a promising strategy against obesity and associated metabolic disorders.
    DOI:  https://doi.org/10.1016/j.neuron.2025.12.002