ArticleJournal of the American Society of Nephrology : JASN2016
Mitochondrial Pathology and Glycolytic Shift during Proximal Tubule Atrophy after Ischemic AKI.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers, 1 of them a synthesis that pooled it.
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Who cites it
229 citing papers in PubMed, 1 synthesis or guideline pooled it, 342 citations in OpenAlex.
- Preclinical models versus clinical renal ischemia reperfusion injury: A systematic review based on metabolic signatures.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022Pooled it
- Advancements in early biomarkers of acute kidney injury: from traditional indicators to a paradigm shift in lactate metabolism.Annals of medicine · 2026Review
- IRAP deficiency preserves renal function and attenuates pathology in aged mice.Clinical science (London, England : 1979) · 2026Article
- Shared inflammatory-metabolic transcriptional effects in tubulointerstitial fibrosis and clear cell renal cell carcinoma.Translational oncology · 2026Article
- The lactate-lactylation axis in acute kidney injury: mechanisms from metabolic reprogramming to epigenetic regulation and clinical therapeutic prospects.International urology and nephrology · 2026Review
- Renal gluconeogenesis: a key metabolic hub in health and kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026Review
- Cardiovascular-kidney-metabolic syndrome as a mitochondrial systems disorder.Nature reviews. Nephrology · 2026Review
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Beyond eGFR and Albuminuria: Biological Pathways and Multiomics in Cardiovascular-Kidney-Metabolic Disease.Kidney international reports · 2026Review
- Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Purine-Metabolism Reprogramming Associated with Failed-Repair Proximal Tubule States in the AKI-to-CKD Transition.Metabolites · 2026Article
- Renal glucose metabolic enzyme expression during AKI-to-CKD transition.International urology and nephrology · 2026Article
- Therapeutic and mechanistic insights on mitochondrial transplantation in kidney disease.Nature reviews. Nephrology · 2026Review
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- Transition to fetal calf serum-free culture enhances kidney proximal tubule cell bioenergetics and allows pharmacological applications.Cell and tissue research · 2026Article
- Glucosamine links hyperglycemia to mTORC1 activation and glucose toxicity in diabetes.JCI insight · 2026Article
- GATM alleviates sepsis-induced acute kidney injury via PDK4-mediated glycolytic reprogramming in renal tubular epithelial cells.Cellular and molecular life sciences : CMLS · 2026Article
- Alkaline Phosphatase Supplementation During Hypothermic and Normothermic Machine Perfusion Improves Metabolic Dysfunction in a Porcine Model of Donor Kidney Preservation.Transplantation direct · 2026Article
169 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
During recovery by regeneration after AKI, proximal tubule cells can fail to redifferentiate, undergo premature growth arrest, and become atrophic. The atrophic tubules display pathologically persistent signaling increases that trigger production of profibrotic peptides, proliferation of interstitial fibroblasts, and fibrosis. We studied proximal tubules after ischemia-reperfusion injury (IRI) to characterize possible mitochondrial pathologies and alterations of critical enzymes that govern energy metabolism. In rat kidneys, tubules undergoing atrophy late after IRI but not normally recovering tubules showed greatly reduced mitochondrial number, with rounded profiles, and large autophagolysosomes. Studies after IRI of kidneys in mice, done in parallel, showed large scale loss of the oxidant-sensitive mitochondrial protein Mpv17L. Renal expression of hypoxia markers also increased after IRI. During early and late reperfusion after IRI, kidneys exhibited increased lactate and pyruvate content and hexokinase activity, which are indicators of glycolysis. Furthermore, normally regenerating tubules as well as tubules undergoing atrophy exhibited increased glycolytic enzyme expression and inhibitory phosphorylation of pyruvate dehydrogenase. TGF-β antagonism prevented these effects. Our data show that the metabolic switch occurred early during regeneration after injury and was reversed during normal tubule recovery but persisted and became progressively more severe in tubule cells that failed to redifferentiate. In conclusion, irreversibility of the metabolic switch, taking place in the context of hypoxia, high TGF-β signaling and depletion of mitochondria characterizes the development of atrophy in proximal tubule cells and may contribute to the renal pathology after AKI.
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