ArticleCell reports2019
Anaerobic Glycolysis Maintains the Glomerular Filtration Barrier Independent of Mitochondrial Metabolism and Dynamics.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.
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Who cites it
105 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Lipid homeostasis in diabetic kidney disease.International journal of biological sciences · 2024Pooled it
- Diabetic kidney disease: emerging mechanistic and nutritional perspectives from the Mediterranean diet-mitochondria axis. A narrative review.The journal of nutrition, health & aging · 2026Review
- Natural products modulate renal metabolic reprogramming in diabetic kidney disease.Journal of translational internal medicine · 2026Article
- TEAD inhibitor induced switch in energy metabolism drives human podocyte injury in vitro.Archives of toxicology · 2026Article
- Podocyte Metabolic Reprogramming and Targeted Therapy.Journal of the American Society of Nephrology : JASN · 2026Review
- MCT1 as a critical regulator of insulin signaling, energy homeostasis and podocyte function.Scientific reports · 2026Article
- Article
- Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies.Frontiers in immunology · 2026Review
- Ectopic lipid deposition in kidney diseases: mechanisms in specific cell types and therapeutic strategies.Frontiers in endocrinology · 2026Review
- From mechanisms to therapies: exploiting epigenetic and post-translational modifications of mitochondrial quality control in diabetic kidney disease.Frontiers in endocrinology · 2026Review
- CX3CL1 deficiency ameliorates acute kidney injury by inhibiting macrophage mitochondrial dysfunction and mtDNA-cGAS-STING signaling.Cell death discovery · 2025Article
- Interactome Quantitation Reveals Non-Energetic Mitochondrial Roles in Cell Type Specialization in Murine Kidney.Molecular & cellular proteomics : MCP · 2025Article
- Mitochondrial morphological aberrations and redistribution in podocytes with glomerular diseases.Renal failure · 2025Article
- Machine Learning-Integrated Explainable Artificial Intelligence Approach for Predicting Steroid Resistance in Pediatric Nephrotic Syndrome: A Metabolomic Biomarker Discovery Study.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Cockayne syndrome mice reflect human kidney disease and are defective in de novo NAD biosynthesis.Cell death and differentiation · 2025Article
- APOL1 risk variants induce metabolic reprogramming of podocytes in patient-derived kidney organoids.Stem cell reports · 2025Article
- Aberrant Glycosylation of IgG in Children With Active Lupus Nephritis Alters Podocyte Metabolism and Causes Podocyte Injury.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Dysregulated Anaerobic Glycolysis in Podocytes is Relevant to the Progression of Focal Segmental Glomerulosclerosis.Kidney international reports · 2025Article
- Targeting TFAM downregulation mediated mtDNA-NLRP3 pathway suppresses TAM infiltration and HCC progression.Oncogene · 2025Article
- Targeting mitochondrial dysfunction: an innovative strategy for treating renal fibrosis.Molecular and cellular biochemistry · 2025Review
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cellular responses induced by mitochondrial dysfunction remain elusive. Intrigued by the lack of almost any glomerular phenotype in patients with profound renal ischemia, we comprehensively investigated the primary sources of energy of glomerular podocytes. Combining functional measurements of oxygen consumption rates, glomerular metabolite analysis, and determination of mitochondrial density of podocytes in vivo, we demonstrate that anaerobic glycolysis and fermentation of glucose to lactate represent the key energy source of podocytes. Under physiological conditions, we could detect neither a developmental nor late-onset pathological phenotype in podocytes with impaired mitochondrial biogenesis machinery, defective mitochondrial fusion-fission apparatus, or reduced mtDNA stability and transcription caused by podocyte-specific deletion of Pgc-1α, Drp1, or Tfam, respectively. Anaerobic glycolysis represents the predominant metabolic pathway of podocytes. These findings offer a strategy to therapeutically interfere with the enhanced podocyte metabolism in various progressive kidney diseases, such as diabetic nephropathy or focal segmental glomerulosclerosis (FSGS).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.