ArticleOncotarget2016
PGC-1α overexpression protects against aldosterone-induced podocyte depletion: role of mitochondria.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Splice modulation of COL4A5 reinstates collagen IV assembly in an organoid model of Alport syndrome.JCI insight · 2026Article
- The Role of Mitochondrial Sirtuins (SIRT3, SIRT4 and SIRT5) in Renal Cell Metabolism: Implication for Kidney Diseases.International journal of molecular sciences · 2024Review
- Hormonal Regulation of Renal Fibrosis.Life (Basel, Switzerland) · 2022Review
- Pathophysiology of diabetic kidney disease: impact of SGLT2 inhibitors.Nature reviews. Nephrology · 2021Review
- Mitochondrial Dysfunction and Diabetic Nephropathy: Nontraditional Therapeutic Opportunities.Journal of diabetes research · 2021Review
- Selective inhibition of arginase-2 in endothelial cells but not proximal tubules reduces renal fibrosis.JCI insight · 2020Article
- Berberine protects against diabetic kidney disease via promoting PGC-1α-regulated mitochondrial energy homeostasis.British journal of pharmacology · 2020Article
- Manipulating Sirtuin 3 pathway ameliorates renal damage in experimental diabetes.Scientific reports · 2020Article
- The Role of PGC-1α and Mitochondrial Biogenesis in Kidney Diseases.Biomolecules · 2020Review
- Aliskiren Reduces the Adrenal Zona Glomerulosa Apoptosis and Autophagy in Wistar Rats with 2K1C Hypertension.International journal of hypertension · 2020Article
- Mitochondrial biogenesis induced by the β2-adrenergic receptor agonist formoterol accelerates podocyte recovery from glomerular injury.Kidney international · 2019Article
- Anaerobic Glycolysis Maintains the Glomerular Filtration Barrier Independent of Mitochondrial Metabolism and Dynamics.Cell reports · 2019Article
- Modulation of energy metabolism and mitochondrial biogenesis by a novel proteoglycan fromRSC advances · 2019Article
- Renal Glomerular Mitochondria Function in Salt-Sensitive Hypertension.Frontiers in physiology · 2019Article
- Knocking down Cabin1 induces glomerular podocyte injury.International urology and nephrology · 2018Article
- The Role of Peroxisome Proliferator-Activated Receptor γ Coactivator 1α (PGC-1α) in Kidney Disease.Seminars in nephrology · 2018Review
- MnTBAP treatment ameliorates aldosterone-induced renal injury by regulating mitochondrial dysfunction and NLRP3 inflammasome signalling.American journal of translational research · 2018Article
- Hyperoside alleviates adriamycin-induced podocyte injury via inhibiting mitochondrial fission.Oncotarget · 2017Article
- Naturally Occurring Compounds: New Potential Weapons against Oxidative Stress in Chronic Kidney Disease.International journal of molecular sciences · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growing evidence has shown that podocyte number is a critical determinant for the development of glomerulosclerosis and progressive renal failure. We previously reported that mitochondrial dysfunction (MtD) is an early event in podocyte injury. Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is an important modulator of mitochondrial biogenesis. Here, we investigated the role of PGC-1α overexpression in podocyte depletion and the involvement of mitochondria in this process. Following chronic aldosterone (Aldo) infusion for 14 days, we observed a remarkable podocyte loss, podocyte phenotypic changes, and albuminuria in WT mice. However, all these abnormalities were significantly attenuated in PGC-1α transgenic mice. Next, we examined mitochondrial function in both genotypes with or without Aldo infusion. As expected, Aldo-induced MtD in glomeruli was markedly improved in PGC-1α transgenic mice. In vitro, Aldo induced podocyte detachment and phenotypic changes in line with MtD in dose- and time-dependent manners. Similarly, ethidium bromide, an inducer of MtD, mimicked Aldo effects on podocyte detachment and phenotypic alterations. Notably, overexpression of PGC-1α in podocytes entirely reversed Aldo-induced podocyte detachment, phenotypic changes, and MtD. Taken together, these findings demonstrate that PGC-1α protects against podocyte depletion and phenotypic changes possibly by maintaining normal mitochondrial function.
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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.