ArticleCell death & disease2016
β-Arrestins promote podocyte injury by inhibition of autophagy in diabetic nephropathy.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 62 citations in OpenAlex.
- Exploring a novel mechanism for targeting β-arrestin-2 in the management of diabetic nephropathy.World journal of diabetes · 2025Article
- From metabolic regulation to kidney protection: β-arrestin 2 as a dual-function therapeutic target.World journal of diabetes · 2025Article
- β-Arrestin-2 enhances endoplasmic reticulum stress-induced glomerular endothelial cell injury by activating transcription factor 6 in diabetic nephropathy.World journal of diabetes · 2024Article
- Blockade of aryl hydrocarbon receptor restricts omeprazole-induced chronic kidney disease.Journal of molecular medicine (Berlin, Germany) · 2024Article
- T-2 Toxin-Mediated β-Arrestin-1 O-GlcNAcylation Exacerbates Glomerular Podocyte Injury via Regulating Histone Acetylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Activation of acetyl-CoA synthetase 2 mediates kidney injury in diabetic nephropathy.JCI insight · 2023Article
- Protective effect of the tunneling nanotube-TNFAIP2/M-sec system on podocyte autophagy in diabetic nephropathy.Autophagy · 2023Article
- Histone modification in podocyte injury of diabetic nephropathy.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Modes of podocyte death in diabetic kidney disease: an update.Journal of nephrology · 2022Review
- Mechanisms of podocyte injury and implications for diabetic nephropathy.Clinical science (London, England : 1979) · 2022Article
- Formyl peptide receptor 1 promotes podocyte injury through regulation of mitogen-activated protein kinase pathways.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- The Effect of Allograft Inflammatory Factor-1 on Inflammation, Oxidative Stress, and Autophagy via miR-34a/ATG4B Pathway in Diabetic Kidney Disease.Oxidative medicine and cellular longevity · 2022Article
- HBx induces hepatocellular carcinogenesis through ARRB1-mediated autophagy to drive the GAutophagy · 2021Article
- Renal Cellular Autophagy in Obesity: Boon or Bane?Seminars in nephrology · 2021Review
- Long non-coding RNA MEG3 promotes cisplatin-induced nephrotoxicity through regulating AKT/TSC/mTOR-mediated autophagy.International journal of biological sciences · 2021Article
- Effect of an Antagonistic Peptide of CCR5 on the Expression of Autophagy-related Genes and β-Arrestin 2 in Lung Tissues of Asthmatic Mice.Allergy, asthma & immunology research · 2021Article
- Yiqi Jiedu Huayu Decoction Alleviates Renal Injury in Rats With Diabetic Nephropathy by Promoting Autophagy.Frontiers in pharmacology · 2021Article
- Article
- The complicated role of mitochondria in the podocyte.American journal of physiology. Renal physiology · 2020Article
- Autophagy in kidney homeostasis and disease.Nature reviews. Nephrology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β-Arrestins are multifunctional proteins originally identified as negative adaptors of G protein-coupled receptors (GPCRs). Emerging evidence has also indicated that β-arrestins can activate signaling pathways independent of GPCR activation. This study was to elucidate the role of β-arrestins in diabetic nephropathy (DN) and hypothesized that β-arrestins contribute to diabetic renal injury by mediating podocyte autophagic process. We first found that both β-arrestin-1 and β-arrestin-2 were upregulated in the kidney from streptozotocin-induced diabetic mice, diabetic db/db mice and kidney biopsies from diabetic patients. We further revealed that either β-arrestin-1 or β-arrestin-2 deficiency (Arrb1(-/-) or Arrb2(-/-)) ameliorated renal injury in diabetic mice. In vitro, we observed that podocytes increased both β-arrestin-1 and β-arrestin-2 expression levels under hyperglycemia condition and further demonstrated that β-arrestin-1 and β-arrestin-2 shared common mechanisms to suppress podocyte autophagy by negative regulation of ATG12-ATG5 conjugation. Collectively, this study for the first time demonstrates that β-arrestin-1 and β-arrestin-2 mediate podocyte autophagic activity, indicating that β-arrestins are critical components of signal transduction pathways that link renal injury to reduce autophagy in DN. Modulation of these pathways may be an innovative therapeutic strategy for treating patients with DN.
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