ArticleCell death discovery2018
Autophagy activation contributes to lipid accumulation in tubular epithelial cells during kidney fibrosis.
Article in Cell death discovery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Lipid homeostasis in diabetic kidney disease.International journal of biological sciences · 2024Pooled it
- Retrospective evaluation of lipiduria in urine from 140 dogs and 74 cats.Journal of veterinary internal medicine · 2026Article
- A TGF-β1/LEF1/β-catenin/JLP network motif regulates autophagy and tubule injury in renal fibrosis.JCI insight · 2026Article
- Autophagy and the peroxisome proliferator-activated receptor signaling pathway: A molecular ballet in lipid metabolism and homeostasis.Molecular and cellular biochemistry · 2025Review
- Hypoxia‑induced SREBP1‑mediated lipogenesis and autophagy promote cell survival via fatty acid oxidation in breast cancer cells.Oncology letters · 2025Article
- UHRF1 promotes calcium oxalate-induced renal fibrosis by renal lipid deposition via bridging AMPK dephosphorylation.Cell biology and toxicology · 2025Article
- ACOT12, a novel factor in the pathogenesis of kidney fibrosis, modulates ACBD5.Experimental & molecular medicine · 2025Article
- The crosstalk of Wnt/β-catenin signaling and p53 in acute kidney injury and chronic kidney disease.Kidney research and clinical practice · 2024Article
- β-catenin-inhibited Sumoylation modification of LKB1 and fatty acid metabolism is critical in renal fibrosis.Cell death & disease · 2024Article
- 5-Fluorouracil induces apoptosis in nutritional deprived hepatocellular carcinoma through mitochondrial damage.Scientific reports · 2024Article
- Article
- GDF15 Interference Regulates Proliferation, Inflammation, and Autophagy of Lipopolysaccharide-induced Mesangial Cells by Inhibiting PI3K/ AKT/mTOR Signaling.Endocrine, metabolic & immune disorders drug targets · 2024Article
- Advances in the study of key cells and signaling pathways in renal fibrosis and the interventional role of Chinese medicines.Frontiers in pharmacology · 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
- Lipid metabolism disorder in diabetic kidney disease.Frontiers in endocrinology · 2024Review
- Zika virus triggers autophagy to exploit host lipid metabolism and drive viral replication.Cell communication and signaling : CCS · 2023Article
- Cell lipid biology in infections: an overview.Frontiers in cellular and infection microbiology · 2023Review
- Frequency of histologic lesions in the kidneys of cats without kidney disease.Journal of feline medicine and surgery · 2022Article
- Expression Profiles of Kidney Mitochondrial Proteome during the Progression of the Unilateral Ureteral Obstruction: Focus on Energy Metabolism Adaptions.Metabolites · 2022Article
- Sulforaphane Protects against Unilateral Ureteral Obstruction-Induced Renal Damage in Rats by Alleviating Mitochondrial and Lipid Metabolism Impairment.Antioxidants (Basel, Switzerland) · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sustained activation of autophagy and lipid accumulation in tubular epithelial cells (TECs) are both associated with the kidney fibrosis progression. Autophagy has been found involved in the lipid metabolism regulation through a bi-directional mechanism of inducing lipolysis as well as promoting lipid droplet formation. However, whether and how autophagy influences lipid accumulation in kidney fibrosis remain unclear. In the current study, we show that UUO-induced lipid accumulation in tubular cells was significantly reduced when the pharmacological inhibitor 3-MA or CQ was administrated both in vivo and in vitro. Of interest, colocalization of LDs and autophagosomes, as well as colocalization of LDs and lysosomes were undetected in UUO-induced fibrotic kidneys, although lysosome function remained robust, indicating the lipid accumulation is lipophagy-lysosome pathway independent. TGF-β1-induced lipid droplets formation in HK-2 cells were decreased when the Beclin-1 expression was silenced, implying that autophagy-upregulated lipid droplets formation is Beclin-1 dependent. Finally, CQ treatment of UUO-induced fibrotic kidneys reduced the expression of α-SMA and tubular cell apoptosis and rescued the expression of E-cadherin, which was associated with the ameliorated lipid deposition. Therefore, our work documented that autophagy promotes lipid droplet formation in TECs in a Beclin-1-dependent manner, which causes renal lipotoxicity and contributes to the progression of kidney fibrosis.
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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.