ArticleJournal of the American Society of Nephrology : JASN2015
Deficient Autophagy Results in Mitochondrial Dysfunction and FSGS.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 1 of them a synthesis that pooled it.
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Who cites it
114 citing papers in PubMed, 1 synthesis or guideline pooled it, 172 citations in OpenAlex.
- Evolutionary patterns and research frontiers in autophagy in podocytopathies: a bibliometric analysis.Frontiers in medicine · 2024Pooled it
- GADD45A may be a potential biomarker associated with endoplasmic reticulum stress in focal segmental glomerulosclerosis.Biochemistry and biophysics reports · 2026Article
- Article
- Chronic exposure to low levels of glyphosate and metals induces kidney dysfunction.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Lipidomic profiling reveals medium-chain acylcarnitines alterations as metabolic signatures in IgA nephropathy.BMC nephrology · 2026Article
- Mitochondrial abnormalities in nondiabetic and nonhypertensive glomerular diseases: a comprehensive review.Molecular and cellular biochemistry · 2026Review
- Macrophage Plasticity and Regulatory Networks During the Transition from Inflammation to Fibrosis in the Kidney.Life (Basel, Switzerland) · 2025Review
- Mitochondrial dysfunction: the hidden catalyst in chronic kidney disease progression.Renal failure · 2025Review
- A novelRenal failure · 2025Article
- Targeting autophagy in autoimmune glomerular diseases.Journal of nephrology · 2025Review
- Dysregulated Anaerobic Glycolysis in Podocytes is Relevant to the Progression of Focal Segmental Glomerulosclerosis.Kidney international reports · 2025Article
- Podocyte dysfunction driven by heme in sickle-cell nephropathy.Scientific reports · 2025Article
- Novel Lipophagy Inducers as Potential Therapeutics for Lipid Metabolism Disorders.ACS chemical biology · 2025Article
- Autophagy: a double-edged sword in ischemia-reperfusion injury.Cellular & molecular biology letters · 2025Review
- Targeting endoplasmic reticulum stress: an innovative therapeutic strategy for podocyte-related kidney diseases.Journal of translational medicine · 2025Review
- Unveiling the therapeutic potential of berberine: its therapeutic role and molecular mechanisms in kidney diseases.Frontiers in pharmacology · 2025Review
- Advances in Focal Segmental Glomerulosclerosis Treatment From the Perspective of the Newest Mechanisms of Podocyte Injury.Drug design, development and therapy · 2025Review
- Association between ATG16L1 rs2241880(T300A) and rs4663421 and ANCA‑associated vasculitis in the Guangxi population of China: Propensity score matching analysis.Biomedical reports · 2025Article
- TRPC6 knockdown-mediated ERK1/2 inactivation alleviates podocyte injury in minimal change disease via upregulating Lon peptidase 1.Renal failure · 2024Article
- Podocyte-targeted therapies - progress and future directions.Nature reviews. Nephrology · 2024Review
54 more citing papers are in PubMed but not listed here.
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9 authors at 4 institutions in 2 countries.
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Abstract
FSGS is a heterogeneous fibrosing disease of the kidney, the cause of which remains poorly understood. In most cases, there is no effective treatment to halt or retard progression to renal failure. Increasing evidence points to mitochondrial dysfunction and the generation of reactive oxygen species in the pathogenesis of CKD. Autophagy, a major intracellular lysosomal degradation system, performs homeostatic functions linked to metabolism and organelle turnover. We prevented normal autophagic pathways in nephrons of mice by mutating critical autophagy genes ATG5 or ATG7 during nephrogenesis. Mutant mice developed mild podocyte and tubular dysfunction within 2 months, profound glomerular and tubular changes bearing close similarity to human disease by 4 months, and organ failure by 6 months. Ultrastructurally, podocytes and tubular cells showed vacuolization, abnormal mitochondria, and evidence of endoplasmic reticulum stress, features that precede the appearance of histologic or clinical disease. Similar changes were observed in human idiopathic FSGS kidney biopsy specimens. Biochemical analysis of podocytes and tubules of 2-month-old mutant mice revealed elevated production of reactive oxygen species, activation of endoplasmic reticulum stress pathways, phosphorylation of p38, and mitochondrial dysfunction. Furthermore, cultured proximal tubule cells isolated from mutant mice showed marked mitochondrial dysfunction and elevated mitochondrial reactive oxygen species generation that was suppressed by a mitochondrial superoxide scavenger. We conclude that mitochondrial dysfunction and endoplasmic reticulum stress due to impaired autophagic organelle turnover in podocytes and tubular epithelium are sufficient to cause many of the manifestations of FSGS in mice.
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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.