bims-celmim Biomed News
on Cellular and mitochondrial metabolism
Issue of 2025–06–01
fifteen papers selected by
Marc Segarra Mondejar
  1. Mitochondrial calcium signaling regulates branched-chain amino acid catabolism in fibrolamellar carcinoma.
  2. Restoring calcium crosstalk between ER and mitochondria promotes intestinal stem cell rejuvenation through autophagy in aged Drosophila.
  3. Reverse electron transport drives metabolic changes in obesity.
  4. Manifold fitting reveals metabolomic heterogeneity and disease associations in UK Biobank populations.
  5. GDP-fucose transporter SLC35C1: a potential regulatory role in cytosolic GDP-fucose and fucosylated glycan synthesis.
  6. Identification of metabolic pathways and serum biomarkers in diabetic cardiomyopathy using untargeted metabolomics.
  7. Adenine nucleotide-dependent Ca2+ buffering by mitochondria in an inorganic phosphate-free medium.
  8. Impact of Drp1 Loss on Organelle Interaction, Metabolism, and Inflammation in Mouse Liver.
  9. Structural and systems characterization of phosphorylation on metabolic enzymes identifies sex-specific metabolic reprogramming in obesity.
  10. Metabolic flux analysis of glioblastoma neural stem cells reveals distinctive metabolic phenotypes in ketogenic conditions.
  11. Nck1 Regulates Glucose Metabolism in Primary Human T Cells.
  12. CoQ imbalance drives reverse electron transport to disrupt liver metabolism.
  13. Genetically encoded fluorescent reporter for polyamines.
  14. Provoking tumor disulfidptosis by single-atom nanozyme via regulating cellular energy supply and reducing power.
  15. Deep learning-driven automated mitochondrial segmentation for analysis of complex transmission electron microscopy images.
  1. Sci Adv. 2025 May 30. 11(22): eadu9512
    Mitochondrial calcium signaling regulates branched-chain amino acid catabolism in fibrolamellar carcinoma.
    Nicole M Marsh, Melissa J S MacEwen, Jane Chea, Heidi L Kenerson, Albert A Kwong, Timothy M Locke, Francisco Javier Miralles, Tanmay Sapre, Natasha Gozali, Madeleine L Hart, Theo K Bammler, James W MacDonald, Lucas B Sullivan, G Ekin Atilla-Gokcumen, Shao-En Ong, John D Scott, Raymond S Yeung, Yasemin Sancak.
      Metabolic adaptations are essential for survival. The mitochondrial calcium uniporter plays a key role in coordinating metabolic homeostasis by regulating mitochondrial metabolic pathways and calcium signaling. However, a comprehensive analysis of uniporter-regulated mitochondrial pathways has remained unexplored. Here, we investigate consequences of uniporter loss and gain of function using uniporter knockout cells and fibrolamellar carcinoma (FLC), which we demonstrate to have elevated mitochondrial calcium levels. We find that branched-chain amino acid (BCAA) catabolism and the urea cycle are uniporter-regulated pathways. Reduced uniporter function boosts expression of BCAA catabolism genes and the urea cycle enzyme ornithine transcarbamylase. In contrast, high uniporter activity in FLC suppresses their expression. This suppression is mediated by the transcription factor KLF15, a master regulator of liver metabolism. Thus, the uniporter plays a central role in FLC-associated metabolic changes, including hyperammonemia. Our study identifies an important role for the uniporter in metabolic adaptation through transcriptional regulation of metabolism and elucidates its importance for BCAA and ammonia metabolism.
    DOI:  https://doi.org/10.1126/sciadv.adu9512
  2. Nat Commun. 2025 May 27. 16(1): 4909
    Restoring calcium crosstalk between ER and mitochondria promotes intestinal stem cell rejuvenation through autophagy in aged Drosophila.
    Yao Zhang, Peng Ma, Saifei Wang, Shuxin Chen, Hansong Deng.
      Breakdown of calcium network is closely associated with cellular aging. Previously, we found that cytosolic calcium (CytoCa2+) levels were elevated while mitochondrial calcium (MitoCa2+) levels were decreased and associated with metabolic shift in aged intestinal stem cells (ISCs) of Drosophila. How MitoCa2+ was decoupled from the intracellular calcium network and whether the reduction of MitoCa2+ drives ISC aging, however, remains unresolved. Here, we show that genetically restoring MitoCa2+ can reverse ISC functional decline and promote intestinal homeostasis by activating autophagy in aged flies. Further studies indicate that MitoCa2+ and Mitochondria-ER contacts (MERCs) form a positive feedback loop via IP3R to regulate autophagy independent of AMPK. Breakdown of this loop is responsible for MitoCa2+ reduction and ISC dysfunction in aged flies. Our results identify a regulatory module for autophagy initiation involving calcium crosstalk between the ER and mitochondria, providing a strategy to treat aging and age-related diseases.
    DOI:  https://doi.org/10.1038/s41467-025-60196-4
  3. Nature. 2025 May 28.
    Reverse electron transport drives metabolic changes in obesity.
      
    Keywords:  Metabolism; Obesity; Physiology
    DOI:  https://doi.org/10.1038/d41586-025-01621-y
  4. Proc Natl Acad Sci U S A. 2025 Jun 03. 122(22): e2500001122
    Manifold fitting reveals metabolomic heterogeneity and disease associations in UK Biobank populations.
    Bingjie Li, Jiaji Su, Runyu Lin, Shing-Tung Yau, Zhigang Yao.
      NMR-based metabolic biomarkers provide comprehensive insights into human metabolism; however, extracting biologically meaningful patterns from such high-dimensional data remains a significant challenge. In this study, we propose a manifold-fitting-based framework to analyze metabolic heterogeneity within the UK Biobank population, utilizing measurements of 251 NMR biomarkers from 212,853 participants. Initially, our method clusters these biomarkers into seven distinct metabolic categories that reflect the modular organization of human metabolism. Subsequent manifold fitting to each category unveils underlying low-dimensional structures, elucidating fundamental variations from basic energy metabolism to hormone-mediated regulation. Importantly, three of these manifolds clearly stratify the population, identifying subgroups with distinct metabolic profiles and associated disease risks. These subgroups exhibit consistent links with specific diseases, including severe metabolic dysregulation and its complications, as well as cardiovascular and autoimmune conditions, highlighting the intricate relationship between metabolic states and disease susceptibility. Supported by strong correlations with demographic factors, clinical measurements, and lifestyle variables, these findings validate the biological relevance of the identified manifolds. By utilizing a geometrically informed approach to dissect metabolic heterogeneity, our framework enhances the accuracy of population stratification and deepens our understanding of metabolic health, potentially guiding personalized interventions and preventive healthcare strategies.
    Keywords:  disease risk prediction; geometric decomposition; manifold fitting; metabolic manifolds; population heterogeneity
    DOI:  https://doi.org/10.1073/pnas.2500001122
  5. FEBS Open Bio. 2025 May 27.
    GDP-fucose transporter SLC35C1: a potential regulatory role in cytosolic GDP-fucose and fucosylated glycan synthesis.
    Edyta Skurska, Mariusz Olczak.
      Glycosylation occurs mainly in the Golgi apparatus, whereas the synthesis of nucleotide sugars occurs in the cytoplasm or nucleus. GDP-fucose in mammalian cells could be produced via de novo and salvage pathways in the cytoplasm; the first one is responsible for about 90% of GDP-fucose in the total pool of this nucleotide sugar in the cell. SLC35C1 (C1) is the primary transporter of GDP-fucose to the Golgi apparatus. In the absence of this transporter, it was proposed that nucleotide sugar could still reach the Golgi apparatus via a SLC35C2, the homologue of SLC35C1. However, simultaneous inactivation of the two transporters did not influence GDP-fucose transport across the Golgi apparatus membranes after external fucose supplementation. In this study, we combined the inactivation of SLC35C1 and enzymes of the GDP-fucose biosynthesis pathways (FCSK, GMDS and TSTA3) to study the impact of double inactivation on the production of nucleotide sugar and fucosylated glycans. We found that a lack of SLC35C1 changed the level of enzymes of both de novo and salvage pathways. Upon fucose supplementation, stimulation of the salvage pathway was remarkably high in the absence of the TSTA3 protein, and the concentration of GDP-fucose increased to millimolar values. In this work, we discovered that simultaneous deficiency of the SLC35C1 protein and TSTA3 enzyme increased GDP-fucose production via the salvage pathway to an even higher level. Finally, we found that nucleotide sugar still accessed the Golgi apparatus and had differential effects on N- and O-glycans.
    Keywords:  FCSK; GMDS; SLC35C1; TSTA3; carbohydrate metabolism; fucosylation
    DOI:  https://doi.org/10.1002/2211-5463.70057
  6. Sci Rep. 2025 May 28. 15(1): 18718
    Identification of metabolic pathways and serum biomarkers in diabetic cardiomyopathy using untargeted metabolomics.
    Jialong Li, Huaming Qiu, Yanjun Wu, Li Su.
      Diabetic cardiomyopathy represents a significant and irreversible chronic cardiovascular complication among diabetic patients. The condition is characterised by early diastolic dysfunction, myocardial fibrosis, cardiac hypertrophy, systolic dysfunction, and other complex pathophysiological events that ultimately lead to heart failure. Untargeted metabolomic analysis represents a powerful tool for the discovery of novel biomarkers. It can not only reveal the metabolic disorder model of diabetic cardiomyopathy, and find specific biomarkers, but also help analyse its pathogenesis and provide new clues for developing treatment strategies. Nevertheless, the precise mechanisms that give rise to diabetic cardiomyopathy remain unclear. In this study, we established a rat model of diabetic cardiomyopathy. We evaluated the model using various established methods, including fasting glucose, glycated hemoglobin, insulin resistance index, cardiac histopathology, and cardiac ultrasound. We then proceeded to identify diabetic cardiomyopathy serum biomarkers by untargeted metabolomics. The potential metabolic pathways of the multiple metabolic differentials were mainly related to amino acid metabolism and arachidonic acid metabolism. Two common metabolites, 5-OxoETE and D-Glutamine, were identified through various cross-comparisons. These two metabolites have good diagnostic ability, especially between DCM vs. CTR, DCM vs. NDCM, and NDCM vs. CTR. These findings may provide new insights into the study of DCM.
    Keywords:  Cardiac ultrasound; Diabetic cardiomyopathy; Diagnostic biomarkers; Ejection fraction; Untargeted metabolomics
    DOI:  https://doi.org/10.1038/s41598-025-98753-y
  7. Biochim Biophys Acta Bioenerg. 2025 May 26. pii: S0005-2728(25)00025-8. [Epub ahead of print]1866(3): 149559
    Adenine nucleotide-dependent Ca2+ buffering by mitochondria in an inorganic phosphate-free medium.
    Anna B Nikiforova, Maxim V Molchanov, Alexey G Kruglov.
      Inorganic phosphate (Pi) is essential for Ca2+ buffering by mitochondria. Adenine nucleotides (AN) are known to strongly increase the Ca2+-retention capacity (CRC) of mitochondria even in the absence of Pi in the medium. Several mechanisms can explain this phenomenon. Here we examined these mechanisms in detail in isolated rat liver mitochondria. We found that, in Pi-free medium, AN dose-dependently increased the CRC. The FOF1-ATP synthase (F-ATPase) inhibitor oligomycin decreased the CRC and the Ca2+ uptake rate to a minor extent. Nuclear magnetic resonance (NMR) analysis showed that Pi in suspensions of oligomycin-treated mitochondria was formed due to AN hydrolysis. In the absence and presence of Ca2+, mitochondria accumulated small and large (50 and > 1000 nmol/mg protein) amounts of Pi, respectively, without detectable accumulation of AN. The average ratio of Ca2+ to Pi accumulated by intact mitochondria in the presence of ADP, ATP, and ATP plus Pi was about 0.68, 1, and 1.25, respectively, or lower. These values correspond to the formation of calcium dihydrogen and hydrogen orthophosphates, and tricalcium phosphate/whitlockite in different proportions. AN increased the CRC in the presence of inhibitors of both F-ATPase and adenylate translocase, the known regulators of the permeability transition pore (PTP). The PTP inhibitor NADH did not increase the CRC in the absence of Pi. Thus, the mechanism of the AN-dependent increase in the CRC in the absence of Pi includes the F-ATPase-independent production of Pi and suppression of the PTP at the site other than F-ATPase and adenylate translocase.
    Keywords:  ADP; ATP; Ca(2+)-retention capacity; Mitochondria; NMR spectroscopy; Permeability transition pore; Phosphate
    DOI:  https://doi.org/10.1016/j.bbabio.2025.149559
  8. Cells. 2025 05 08. pii: 679. [Epub ahead of print]14(10):
    Impact of Drp1 Loss on Organelle Interaction, Metabolism, and Inflammation in Mouse Liver.
    Lixiang Wang, Seiji Nomura, Nao Hasuzawa, Sadaki Yokota, Ayako Nagayama, Kenji Ashida, Junjiro Rikitake, Yoshinori Moriyama, Masatoshi Nomura, Ken Yamamoto.
      Dynamin-related protein 1 (Drp1) is a crucial player in mitochondrial fission and liver function. The interactions between mitochondria, endoplasmic reticulum (ER), and lipid droplets (LDs) are fundamental for lipid metabolism. This study utilized liver-specific Drp1 knockout (Drp1LiKO) mice to investigate the effects of Drp1 deficiency on organelle interactions, metabolism, and inflammation. Our analysis revealed disrupted interactions between mitochondria and LDs, as well as altered interactions among ER, mitochondria, and LDs in Drp1LiKO mice. Through mass spectrometry and microarray analysis, we identified changes in lipid profiles and perturbed expression of lipid metabolism genes in the livers of Drp1LiKO mice. Further in vitro experiments using primary hepatocytes from Drp1LiKO mice confirmed disturbances in lipid metabolism and increased inflammation. These findings highlight the critical involvement of Drp1 in regulating organelle interactions for efficient lipid metabolism and overall liver health. Targeting Drp1-mediated organelle interactions may offer potential for developing therapies for liver diseases associated with disrupted lipid metabolism.
    Keywords:  dynamin-related protein 1; lipid metabolism; liver inflammation; organelle interaction
    DOI:  https://doi.org/10.3390/cells14100679
  9. Mol Cell. 2025 May 21. pii: S1097-2765(25)00412-5. [Epub ahead of print]
    Structural and systems characterization of phosphorylation on metabolic enzymes identifies sex-specific metabolic reprogramming in obesity.
    Tigist Y Tamir, Shreya Chaudhary, Annie X Li, Sonia E Trojan, Cameron T Flower, Paula Vo, Yufei Cui, Jeffrey C Davis, Rachit Mukkamala, Francesca N Venditti, Alissandra L Hillis, Alex Toker, Matthew G Vander Heiden, Jessica B Spinelli, Norman J Kennedy, Roger J Davis, Forest M White.
      Coordination of adaptive metabolism through signaling networks is essential for cellular bioenergetics and homeostasis. Phosphorylation of metabolic enzymes provides a rapid, efficient, and dynamic mechanism to regulate metabolic networks. Our structural analysis stratified phosphosites on metabolic enzymes based on proximity to functional and dimerization domains. Most phosphosites occur on oxidoreductases and are enriched near substrate, cofactor, active sites, or dimer interfaces. Despite low stoichiometry, phosphotyrosine (pY) is overrepresented in functional domains. Using high-fat diet (HFD)-induced obesity in C57BL/6J mice and multiomics, we measured HFD-induced sex-specific dysregulation of pY and metabolites, which was reversible with the antioxidant butylated hydroxyanisole (BHA). Computational modeling revealed predictive pY sites for HFD- or BHA-induced metabolite changes. We characterized functional roles for predictive pY sites on glutathione S-transferase pi 1 (GSTP1), isocitrate dehydrogenase 1 (IDH1), and uridine monophosphate synthase (UMPS) using CRISPR interference (CRISPRi) rescue and stable isotope tracing. Our findings reveal mechanisms whereby cellular signaling fine-tunes enzyme activity and metabolism.
    Keywords:  GSTP1; IDH1; UMPS; cell signaling; computational modelling; metabolism; metabolomics; obesity; oxidative stress response; phosphoproteomics
    DOI:  https://doi.org/10.1016/j.molcel.2025.05.007
  10. Sci Rep. 2025 May 28. 15(1): 18736
    Metabolic flux analysis of glioblastoma neural stem cells reveals distinctive metabolic phenotypes in ketogenic conditions.
    Anna Rushin, Aleezeh Shaikh, Callie Hardin, Loic P Deleyrolle, Matthew E Merritt.
      Glioblastomas (GBM) are the most prevalent primary brain tumors, affecting 5 in every 100,000 people. GBMs optimize proliferation through adaptive cellular metabolism, frequently exploiting the Warburg effect by increasing aerobic glycolysis and glucose utilization to facilitate rapid cell growth. This disproportionate reliance on glucose has driven interest in using the ketogenic diet (KD) as a treatment for GBM. In this study, we explored metabolic flux in three primary human GBM cell samples using a media simulating a KD. Flux analysis using a detailed metabolic modeling approach revealed three unique metabolic phenotypes in the patient GBMs that correlated with cell viability. Notably, these phenotypes are apparent in the flux modeling, but were not evidenced by changes in the metabolite pool sizes. This variability in metabolic flux may underlie the inconsistent results observed in preclinical and clinical studies using the KD as a treatment paradigm.
    Keywords:  Cancer biology; Glioblastoma; Isotopic analysis; Ketogenesis; Metabolism
    DOI:  https://doi.org/10.1038/s41598-025-02124-6
  11. Immunology. 2025 May 27.
    Nck1 Regulates Glucose Metabolism in Primary Human T Cells.
    Araya Rattanasri, Pussadee Paensuwan, Wolfgang W W A Schamel, Sutatip Pongcharoen, Jatuporn Ngoenkam.
      Non-catalytic region of tyrosine kinase 1 (Nck1) is an adaptor protein found in many cell types and plays several functions. In T cells, Nck1 is functionally associated with a T cell receptor (TCR)-mediated actin rearrangement, insulin signalling, PI3K/Akt/mTOR pathway, and lipid production. However, the role of Nck1 in regulating glucose metabolism in T cells is still largely unknown. In the present study, the role of Nck1 in glucose metabolism in primary human T cells was investigated. Plasmid encoding Nck1-specific short hairpin RNA (shRNA) was delivered to primary T cells to mediate Nck1 silencing. Plasmids encoding Nck1-specific short hairpin RNA (shRNA) were delivered to primary human T cells to mediate Nck1 silencing. Nck1-knockdown (N1KD) cells were analysed for processes related to glucose metabolism and function. Despite an increased expression of glucose transporter 1 (GLUT1) in N1KD cells, these cells exhibited impaired glucose uptake and ATP production, indicating dysfunction of GLUT1 or altered intracellular glucose metabolism. Nck1 depletion disrupted metabolic signalling characterised by reduced TXNIP and phosphoribosomal protein S6 (pS6) levels, along with an increased phosphorylation of Akt and AMPK. The reduced extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) found in N1KD cells indicated impaired glycolysis and oxidative phosphorylation. Functionally, these metabolic alterations were associated with impaired T cell activation, reduced proliferation, and increased apoptosis. Collectively, Nck1 critically regulated glucose metabolism in T cells, linking metabolic reprogramming to immune function and cell survival.
    Keywords:  Nck1; T cell; T cell activation; T cell signalling; glucose metabolism
    DOI:  https://doi.org/10.1111/imm.13950
  12. Nature. 2025 May 28.
    CoQ imbalance drives reverse electron transport to disrupt liver metabolism.
    Renata L S Goncalves, Zeqiu Branden Wang, Jillian K Riveros, Güneş Parlakgül, Karen E Inouye, Grace Yankun Lee, Xiaorong Fu, Jani Saksi, Clement Rosique, Sheng Tony Hui, Mar Coll, Ana Paula Arruda, Shawn C Burgess, Isabel Graupera, Gökhan S Hotamışlıgil.
      Mitochondrial reactive oxygen species (mROS) are central to physiology1,2. Excess mROS production has been associated with several disease states2,3; however, the precise sources, regulation and mechanism of generation in vivo remain unclear, which limits translational efforts. Here we show that in obesity, hepatic coenzyme Q (CoQ) synthesis is impaired, which increases the CoQH2 to CoQ (CoQH2/CoQ) ratio and drives excessive mROS production through reverse electron transport (RET) from site IQ in complex I. Using multiple complementary genetic and pharmacological models in vivo, we demonstrate that RET is crucial for metabolic health. In patients with steatosis, the hepatic CoQ biosynthetic program is also suppressed, and the CoQH2/CoQ ratio positively correlates with disease severity. Our data identify a highly selective mechanism for pathological mROS production in obesity, which can be targeted to protect metabolic homeostasis.
    DOI:  https://doi.org/10.1038/s41586-025-09072-1
  13. Nat Commun. 2025 May 27. 16(1): 4921
    Genetically encoded fluorescent reporter for polyamines.
    Pushkal Sharma, Colin Y Kim, Heather R Keys, Shinya Imada, Alex B Joseph, Luke Ferro, Tenzin Kunchok, Rachel Anderson, Yulin Sun, Ömer H Yilmaz, Jing-Ke Weng, Ankur Jain.
      Polyamines are abundant and evolutionarily conserved metabolites that are essential for life. Dietary polyamine supplementation extends life-span and health-span. Dysregulation of polyamine homeostasis is linked to Parkinson's disease and cancer, driving interest in therapeutically targeting this pathway. However, measuring cellular polyamine levels, which vary across cell types and states, remains challenging. We introduce a genetically encoded polyamine reporter for real-time measurement of polyamine concentrations in single living cells. This reporter utilizes the polyamine-responsive ribosomal frameshift motif from the OAZ1 gene. We demonstrate broad applicability of this approach and reveal dynamic changes in polyamine levels in response to genetic and pharmacological perturbations. Using this reporter, we conduct a genome-wide CRISPR screen and uncover an unexpected link between mitochondrial respiration and polyamine import, which are both risk factors for Parkinson's disease. By offering a lens to examine polyamine biology, this reporter may advance our understanding of these ubiquitous metabolites and accelerate therapy development.
    DOI:  https://doi.org/10.1038/s41467-025-60147-z
  14. Nat Commun. 2025 May 26. 16(1): 4877
    Provoking tumor disulfidptosis by single-atom nanozyme via regulating cellular energy supply and reducing power.
    Wenxin Yu, Duo Jin, Yajie Zhang, Shenghu Wang, Jiaji Yu, Manman Liu, Yi Dai, Yichen Yin, Junjie Cheng, Yangzhong Liu.
      Disulfidptosis, a recently identified form of programmed cell death, is initiated by depletion of endogenous nicotinamide adenine dinucleotide phosphate (NADPH) under glucose starvation. Tumor cells, owing to their heightened requirements of energy and nutrients, are more susceptible to disulfidptosis than normal cells. Here, we introduced an effective strategy to induce tumor disulfidptosis via interrupting cellular energy supply and reducing power by integrating a copper single-atom nanozyme (CuSAE) and glucose oxidase (GOx). GOx induces glucose starvation, impeding generation of NADPH through pentose phosphate pathway (PPP). CuSAE mimics NADPH oxidase, depleting existing NADPH, which intensifies the blockade of disulfide reduction and efficiently triggers disulfidptosis of tumor cells. Furthermore, CuSAE exhibits peroxidase- and glutathione oxidase-mimicking activities, catalyzing generation of •OH radical and depletion cellular GSH, which enhances oxidative stress and exacerbates cell damage. Disulfidptosis is confirmed as the predominant type of cell death induced by GOx/CuSAE. In vivo assays demonstrated the high antitumor potency of GOx/CuSAE in treating with female tumor-bearing mice, with minimal systemic toxicity observed. This work introduces a promising strategy for designing antitumor agents by inducing disulfidptosis. The enzyme hybrids that combine nanozymes and natural enzymes offer a feasible approach to achieve this multifaceted therapeutic goal.
    DOI:  https://doi.org/10.1038/s41467-025-60015-w
  15. Sci Rep. 2025 May 30. 15(1): 19076
    Deep learning-driven automated mitochondrial segmentation for analysis of complex transmission electron microscopy images.
    Chan Jang, Hojun Lee, Jaejun Yoo, Haejin Yoon.
      Mitochondria are central to cellular energy production and regulation, with their morphology tightly linked to functional performance. Precise analysis of mitochondrial ultrastructure is crucial for understanding cellular bioenergetics and pathology. While transmission electron microscopy (TEM) remains the gold standard for such analyses, traditional manual segmentation methods are time-consuming and prone to error. In this study, we introduce a novel deep learning framework that combines probabilistic interactive segmentation with automated quantification of mitochondrial morphology. Leveraging uncertainty analysis and real-time user feedback, the model achieves comparable segmentation accuracy while reducing analysis time by 90% compared to manual methods. Evaluated on both benchmark Lucchi++ datasets and real-world TEM images of mouse skeletal muscle, the pipeline not only improved efficiency but also identified key pathological differences in mitochondrial morphology between wild-type and mdx mouse models of Duchenne muscular dystrophy. This automated approach offers a powerful, scalable tool for mitochondrial analysis, enabling high-throughput and reproducible insights into cellular function and disease mechanisms.
    Keywords:  Automated quantification; Deep learning segmentation; Interactive segmentation; Mitochondrial morphology; Transmission electron microscopy imaging; Uncertainty analysis
    DOI:  https://doi.org/10.1038/s41598-025-03311-1
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