Bisphenol A induces coronary endothelial cell necroptosis by activating RIP3/CamKII dependent pathway.

ABSTRACT: Epidemiological studies link long term exposure to xenoestrogen Bisphenol-A to adverse cardiovascular effects. Our previous results show that BPA induces hypertension by a mechanism involving CamKII activation and increased redox stress caused by eNOS uncoupling. Recently, CamKII sustained activation has been recognized as a central mediator of programmed cell death in cardiovascular diseases, including necroptosis. However, the role of necroptosis in cardiac response to BPA had not yet been explored. Mice exposed to BPA for 16 weeks showed altered heart function, electrical conduction, and increased blood pressure. Besides, a stress test showed ST-segment depression, indicative of cardiac ischemia. The hearts exhibited cardiac hypertrophy and reduced vascularization, interstitial edema, a

SUBMITTER: Reventun P 

PROVIDER: S-EPMC7060177 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature