ArticleMolecular biology of the cell2016
Angiotensin II down-regulates nephrin-Akt signaling and induces podocyte injury: roleof c-Abl.
Article in Molecular biology of the cell, 2016. 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 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Sodium-Glucose Cotransporter-2 Inhibitors in Diabetes and Beyond: Mechanisms, Pleiotropic Benefits, and Clinical Use-Reviewing Protective Effects Exceeding Glycemic Control.Molecules (Basel, Switzerland) · 2025Review
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
- TangNaikang Formula Alleviates Podocyte Injury in Diabetic Nephropathy by Modulating the SHIP2/PI3K/AKT Pathway.Journal of diabetes research · 2025Article
- Klotho Stabilizes the Podocyte Actin Cytoskeleton in Idiopathic Membranous Nephropathy through Regulating the TRPC6/CatL Pathway.American journal of nephrology · 2024Article
- Unveiling Angiotensin II and Losartan-Induced Gene Regulatory Networks Using Human Urine-Derived Podocytes.International journal of molecular sciences · 2023Article
- Sirt6 deficiency contributes to mitochondrial fission and oxidative damage in podocytes via ROCK1-Drp1 signalling pathway.Cell proliferation · 2022Article
- Release of HMGB1 in Podocytes Exacerbates Lipopolysaccharide-Induced Acute Kidney Injury.Mediators of inflammation · 2021Article
- Critical roles of PI3K/Akt/NF‑κB survival axis in angiotensin II‑induced podocyte injury.Molecular medicine reports · 2019Article
- [Angiotensin Ⅱ induces apoptosis of HEK293T cells by up-regulating Cyr61 expression].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- Molecular Mechanisms of Kidney Injury and Repair in Arterial Hypertension.International journal of molecular sciences · 2019Review
- Identification of the Transcriptional Networks and the Involvement in Angiotensin II-Induced Injury after CRISPR/Cas9-Mediated Knockdown of Cyr61 in HEK293T Cells.Mediators of inflammation · 2019Article
- Engineering renal epithelial cells: programming and directed differentiation towards glomerular podocyte's progenitor and mature podocyte.American journal of translational research · 2019Review
- Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.Cell death & disease · 2018Article
- Proteinuric Kidney Diseases: A Podocyte's Slit Diaphragm and Cytoskeleton Approach.Frontiers in medicine · 2018Review
- Nephrin Signaling in the Podocyte: An Updated View of Signal Regulation at the Slit Diaphragm and Beyond.Frontiers in endocrinology · 2018Review
- Angiotensin II induces cholesterol accumulation and injury in podocytes.Scientific reports · 2017Article
- Dab1 Contributes to Angiotensin II-Induced Apoptosis via p38 Signaling Pathway in Podocytes.BioMed research international · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Recent studies have shown that nephrin plays a vital role in angiotensin II (Ang II)-induced podocyte injury and thus contributes to the onset of proteinuria and the progression of renal diseases, but its specific mechanism remains unclear. c-Abl is an SH2/SH3 domain-containing nonreceptor tyrosine kinase that is involved in cell survival and regulation of the cytoskeleton. Phosphorylated nephrin is able to interact with molecules containing SH2/SH3 domains, suggesting that c-Abl may be a downstream molecule of nephrin signaling. Here we report that Ang II-infused rats developed proteinuria and podocyte damage accompanied by nephrin dephosphorylation and minimal interaction between nephrin and c-Abl. In vitro, Ang II induced podocyte injury and nephrin and Akt dephosphorylation, which occurred in tandem with minimal interaction between nephrin and c-Abl. Moreover, Ang II promoted c-Abl phosphorylation and interaction between c-Abl and SH2 domain-containing 5'-inositol phosphatase 2 (SHIP2). c-Abl small interfering RNA (siRNA) and STI571 (c-Abl inhibitor) provided protection against Ang II-induced podocyte injury, suppressed the Ang II-induced c-Abl-SHIP2 interaction and SHIP2 phosphorylation, and maintained a stable level of nephrin phosphorylation. These results indicate that c-Abl is a molecular chaperone of nephrin signaling and the SHIP2-Akt pathway and that the released c-Abl contributes to Ang II-induced podocyte injury.
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