Why the study?
Angiotensin II induces hypertension, vascular thickening, and atherosclerosis, but the effects of ANGPTL7 in AngII-induced hypertension needed validation.
ANGPTL7 downregulation reverses AngII-induced proliferation and inflammation in vascular smooth muscle cells, suggesting it as a potential therapeutic target for hypertension.
ANGPTL7 downregulation may blunt AngII-driven vascular cell proliferation; hypothesis-generating for targeted hypertension therapies.
INTRODUCTION: Angiotensin II (AngII) induces hypertension and pathophysiological vascular thickening and atherosclerosis. This study aims to validate the effects of Angiopoietin-like 7 (ANGPTL7) in AngII-induced hypertension. METHODS: ANGPTL7 in blood samples were determined by quantitative real-time polymerase chain reaction. AngII-induced cell growth were detected by CCK-8. Cell cycle arrest and cell apoptosis by downregulation of ANGPTL7 were detected by flow cytometric assay. AngII-induced inflammation was evaluated by Western blotting and ELISA. RESULTS: ANGPTL7 was highly expressed in patients with hypertension. AngII promoted cell viability and the expression level of ANGPTL7 in vascular smooth muscle cells (VSMC). Downregulation of ANGPTL7 inhibited AngII-induced cell proliferation and cell inflammation. Moreover, ANGPTL7 expression decreases also promoted cell apoptosis. CONCLUSIONS: Downregulation of ANGPTL7 reversed AngII-induced cell proliferation and cell inflammation and promoted apoptosis in AngII-induced VSMC cells. Therefore, ANGPTL7 can be a potential target in AngII-induced hypertension.
No takes yet. Share an insight, caveat, or question.
Zhao et al. (2019) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: