ArticleJournal of the American Society of Nephrology : JASN2016
Autophagy Induces Prosenescent Changes in Proximal Tubular S3 Segments.
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 67 papers.
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Who cites it
67 citing papers in PubMed, 97 citations in OpenAlex.
- Magnesium Attenuates Renal Senescence and Fibrosis With Reduced DNA Damage Response and H3K4me3 Enrichment at the p16FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Protective effects of gastrodin against bisphenol A-induced dopaminergic dysregulation and cognitive impairment in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Review
- Hypoxia-Inducible Factor-1α Drives Cellular Senescence via Autophagy Activation to Promote Acute Kidney Injury-to-CKD Transition.American journal of nephrology · 2026Article
- Yiqi-Wenyang-Tiaoshen Decoction Reduces Cisplatin-Induced Acute Kidney Injury in Rats Through Autophagy and Apoptosis Signaling Pathways Based on Network Pharmacology and Experimental Validation.Mediators of inflammation · 2026Article
- Autophagy Related 5 Promotes Mitochondrial Fission and Inflammation via HSP90-HIF-1α-Mediated Glycolysis in Kidney Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Integrated multiomics analysis identifies potential biomarkers and therapeutic targets for autophagy associated AKI to CKD transition.Scientific reports · 2025Article
- Targeting senescence to prevent diabetic kidney disease: Exploring molecular mechanisms and potential therapeutic targets for disease management.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Macrophage autophagy protects against acute kidney injury by inhibiting renal inflammation through the degradation of TARM1.Autophagy · 2025Article
- Dynamic regulation of proximal tubular autophagy from injury to repair after ischemic kidney damage.Cellular & molecular biology letters · 2024Article
- Kidney Aging and Chronic Kidney Disease.International journal of molecular sciences · 2024Review
- Transcriptome Analysis of BAFF/BAFF-R System in Murine Nephrotoxic Serum Nephritis.International journal of molecular sciences · 2024Article
- Article
- Atg5 deficiency in macrophages protects against kidney fibrosis via the CCR6-CCL20 axis.Cell communication and signaling : CCS · 2024Article
- HIF-1 contributes to autophagy activation via BNIP3 to facilitate renal fibrosis in hypoxia in vitro and UUO in vivo.American journal of physiology. Cell physiology · 2024Article
- Inspiring Tactics with the Improvement of Mitophagy and Redox Balance for the Development of Innovative Treatment against Polycystic Kidney Disease.Biomolecules · 2024Review
- The pro-fibrotic role of autophagy in renal intrinsic cells: mechanisms and therapeutic potential in chronic kidney disease.Frontiers in cell and developmental biology · 2024Review
- Tubular cell senescence promotes maladaptive kidney repair and chronic kidney disease after cisplatin nephrotoxicity.JCI insight · 2023Article
- Review
- Autophagy in acute kidney injury and maladaptive kidney repair.Burns & trauma · 2023Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evidence suggests that autophagy promotes the development of cellular senescence. Because cellular senescence contributes to renal aging and promotes the progression from AKI to CKD, we investigated the potential effect of tubular autophagy on senescence induction. Compared with kidneys from control mice, kidneys from mice with conditional deletion of autophagy-related 5 (Atg5) for selective ablation of autophagy in proximal tubular S3 segments (Atg5(Δ) (flox/) (Δ) (flox)) presented with significantly less tubular senescence, reduced interstitial fibrosis, and superior renal function 30 days after ischemia/reperfusion injury. To correlate this long-term outcome with differences in the early injury process, kidneys were analyzed 2 hours and 3 days after reperfusion. Notably, compared with kidneys of control mice, Atg5(Δ) (flox/) (Δ) (flox) kidneys showed more cell death in outer medullary S3 segments at 2 hours but less tubular damage and inflammation at day 3. These data suggest that the lack of autophagy prevents early survival mechanisms in severely damaged tubular cells. However, if such compromised cells persist, then they may lead to maladaptive repair and proinflammatory changes, thereby facilitating the development of a senescent phenotype and CKD.
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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.