ArticleAmerican journal of physiology. Heart and circulatory physiology2006
ANG II induces apoptosis of human vascular smooth muscle via extrinsic pathway involving inhibition of Akt phosphorylation and increased FasL expression.
Article in American journal of physiology. Heart and circulatory physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 44 citations in OpenAlex.
- Targeting Nupr1-Mediated p53 Mitochondrial Sequestration Alleviates Aortic Dissection by Restoring the Gadd45b-Dependent Survival Program.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Integrated Network Pharmacology, Single-Cell Transcriptomics Unveil the Mechanistic Role of Morusin in Aortic Dissection.Journal of cellular and molecular medicine · 2026Article
- Defective autophagy in vascular smooth muscle cells promote uremic accelerated atherosclerosis.Renal failure · 2025Article
- Inhibition of smooth muscle cell death by Angiotensin 1-7 protects against abdominal aortic aneurysm.Bioscience reports · 2023Article
- Targeted Inhibition of Matrix Metalloproteinase-8 Prevents Aortic Dissection in a Murine Model.Cells · 2022Article
- D-Limonene Is a Potential Monoterpene to Inhibit PI3K/Akt/IKK-α/NF-κB p65 Signaling Pathway in Coronavirus Disease 2019 Pulmonary Fibrosis.Frontiers in medicine · 2021Article
- The Impact of the Renin-Angiotensin-Aldosterone System on Inflammation, Coagulation, and Atherothrombotic Complications, and to Aggravated COVID-19.Frontiers in pharmacology · 2021Review
- Baicalin alleviates bleomycin‑induced pulmonary fibrosis and fibroblast proliferation in rats via the PI3K/AKT signaling pathway.Molecular medicine reports · 2020Article
- Angiotensin II inhibits apoptosis of mouse aortic smooth muscle cells through regulating the circNRG-1/miR-193b-5p/NRG-1 axis.Cell death & disease · 2019Article
- The transient receptor potential vanilloid-3 regulates hypoxia-mediated pulmonary artery smooth muscle cells proliferation via PI3K/AKT signaling pathway.Cell proliferation · 2018Article
- BMP4 protects rat pulmonary arterial smooth muscle cells from apoptosis by PI3K/AKT/Smad1/5/8 signaling.International journal of molecular sciences · 2014Article
- Cardioprotective microRNAs.Pediatric cardiology · 2011Article
- AKT-ing via microRNA.Cell cycle (Georgetown, Tex.) · 2010Article
- MicroRNA-21 is a downstream effector of AKT that mediates its antiapoptotic effects via suppression of Fas ligand.The Journal of biological chemistry · 2010Article
- Aortic cell apoptosis in rat primary aldosteronism model.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2010Article
- The effects of mesenchymal stem cells on c-kit up-regulation and cell-cycle re-entry of neonatal cardiomyocytes are mediated by activation of insulin-like growth factor 1 receptor.Molecular and cellular biochemistry · 2009Article
- Angiotensin II-mediated oxidative DNA damage accelerates cellular senescence in cultured human vascular smooth muscle cells via telomere-dependent and independent pathways.Circulation research · 2008Article
- Differential regulation of Akt, caspases and MAP kinases underlies smooth muscle cell apoptosis during aortic remodelling in SHR treated with amlodipine.British journal of pharmacology · 2007Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In addition to well-documented vascular growth-promoting effects, ANG II exerts proapoptotic effects that are poorly understood. IGF-1 is a potent survival factor for human vascular smooth muscle cells (hVSMC), and its antiapoptotic effects are mediated via the IGF-1 receptor (IGF-1R) through a signaling pathway involving phosphatidylinositol 3-kinase and Akt. We hypothesized that there would be cross talk between ANG II proapoptotic effects and IGF-1 survival effects in hVSMC. To investigate ANG II-induced apoptosis and the potential involvement of IGF-1, we exposed quiescent and nonquiescent hVSMC to ANG II. ANG II induced apoptosis only in nonquiescent cells but stimulated hypertrophy in quiescent cells. ANG II-induced apoptosis was characterized by marked inhibition of Akt phosphorylation and stimulation of membrane Fas ligand (FasL) expression, caspase-8 activation, and a reduction in soluble FasL expression. Adenovirally mediated overexpression of Akt rescued hVSMC from ANG II-induced apoptosis. IGF-1R activation increased Akt phosphorylation and soluble FasL expression, and these effects were completely blocked by coincubating hVSMC with ANG II. In conclusion, ANG II-induced apoptosis of hVSMC is characterized by marked inhibition of Akt phosphorylation and stimulation of an extrinsic cell death signaling pathway via upregulation of membrane FasL expression, caspase-8 activation, and a reduction in soluble FasL expression. Furthermore, ANG II antagonizes the antiapoptotic effect of IGF-1 by blocking its ability to increase Akt phosphorylation and soluble FasL. These findings provide novel insights into ANG II-induced apoptotic signaling and have significant implication for understanding ANG II-induced remodeling in hypertension and atherosclerosis.
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