ArticleAutophagy2016
Persistent activation of autophagy in kidney tubular cells promotes renal interstitial fibrosis during unilateral ureteral obstruction.
Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 2 of them syntheses that pooled it.
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Who cites it
170 citing papers in PubMed, 2 syntheses or guidelines pooled it, 243 citations in OpenAlex.
- Beneficial effects of cell-derived exosomes on diabetic nephropathy: a systematic review and meta-analysis of preclinical evidence.Acta diabetologica · 2025Pooled it
- Transcriptome meta-analysis and validation to discovery of hub genes and pathways in focal and segmental glomerulosclerosis.BMC nephrology · 2024Pooled it
- KLF transcription factors in metabolic kidney disease: from podocyte protection to tubulointerstitial fibrosis.International urology and nephrology · 2026Review
- Myofibroblast- specific autophagy drives cyst growth in autosomal dominant polycystic kidney disease.Cell communication and signaling : CCS · 2026Article
- A TGF-β1/LEF1/β-catenin/JLP network motif regulates autophagy and tubule injury in renal fibrosis.JCI insight · 2026Article
- Microvascular autophagy and caspase-3 activation are central regulators of renal fibrosis after ischemia-reperfusion.JCI insight · 2026Article
- Peroxisomal Degradation Correlates with the Progression of Kidney Injury in a UUO Mouse Model.Biology · 2026Article
- Small molecules targeting regulated cell death for chronic kidney disease therapy.Journal of pharmaceutical analysis · 2026Review
- The AMPK/NRF2/FOXO Axis in CKD-Molecular and Clinical Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- LncRNA P4HA2-AS1 drives renal interstitial fibrosis via trim32-mediated k63 ubiquitination of ULK1 and autophagic dysregulation.Communications biology · 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
- Lead-Induced Nephrotoxicity and Its Therapeutic Interventions: An Updated Review.Biological trace element research · 2026Review
- Cell-state- and compartment-dependent PI3K/Akt redox signaling in chronic kidney disease: mechanisms and translational implications.Frontiers in pharmacology · 2026Review
- Review
- Targeting autophagy in autoimmune glomerular diseases.Journal of nephrology · 2025Review
- Targeting mitochondrial dysfunction: an innovative strategy for treating renal fibrosis.Molecular and cellular biochemistry · 2025Review
- Risk Factors of Histopathological Crescent Formation in Pediatric IgA Vasculitis Nephritis.Medicina (Kaunas, Lithuania) · 2025Article
- Preclinical evidence of the effect of icariin on diabetic nephropathy: a systematic review and meta-analysis.Diabetology & metabolic syndrome · 2025Review
- Protective effect ofBiomedical reports · 2025Article
- TUT7-Mediated Uridine Degradation of MCPIP1 in the Pterygium to Regulate TRAF6-Mediated Autophagy.Investigative ophthalmology & visual science · 2025Article
110 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
Renal fibrosis is the final, common pathway of end-stage renal disease. Whether and how autophagy contributes to renal fibrosis remains unclear. Here we first detected persistent autophagy in kidney proximal tubules in the renal fibrosis model of unilateral ureteral obstruction (UUO) in mice. UUO-associated fibrosis was suppressed by pharmacological inhibitors of autophagy and also by kidney proximal tubule-specific knockout of autophagy-related 7 (PT-Atg7 KO). Consistently, proliferation and activation of fibroblasts, as indicated by the expression of ACTA2/α-smooth muscle actin and VIM (vimentin), was inhibited in PT-Atg7 KO mice, so was the accumulation of extracellular matrix components including FN1 (fibronectin 1) and collagen fibrils. Tubular atrophy, apoptosis, nephron loss, and interstitial macrophage infiltration were all inhibited in these mice. Moreover, these mice showed a specific suppression of the expression of a profibrotic factor FGF2 (fibroblast growth factor 2). In vitro, TGFB1 (transforming growth factor β 1) induced autophagy, apoptosis, and FN1 accumulation in primary proximal tubular cells. Inhibition of autophagy suppressed FN1 accumulation and apoptosis, while enhancement of autophagy increased TGFB1-induced-cell death. These results suggest that persistent activation of autophagy in kidney proximal tubules promotes renal interstitial fibrosis during UUO. The profibrotic function of autophagy is related to the regulation on tubular cell death, interstitial inflammation, and the production of profibrotic factors.
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Registered trials
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.