Caspase-1 regulates Ang II-induced cardiomyocyte hypertrophy via up-regulation of IL-1β. Issue 2 (16th March 2018)

• Record Type: Journal Article
• Authors: Bai, Yunlong; Sun, Xi; Chu, Qun; Li, Anqi; Qin, Ying; Li, Yanyao; Yue, Er; Wang, Hui; Li, GuiYang; Zahra, Syeda Madiha; Dong, Chaorun; Jiang, Yanan
• Is Part Of: Bioscience reports. Volume 38:Issue 2(2018)
• Publication Date: 2018-03-16
• Subjects: Cardiac hypertrophy -- caspase-1 -- IL-1β -- pyroptosis; Molecular biology -- Periodicals; Cytology -- Periodicals; 572.8
• DOI: 10.1042/BSR20171438
• Languages: English
• ISSNs: 0144-8463

Abstract

Abstract : Cardiac hypertrophy is a compensatory response to stress or stimuli, which results in arrhythmia and heart failure. Although multiple molecular mechanisms have been identified, cardiac hypertrophy is still difficult to treat. Pyroptosis is a caspase-1-dependent pro-inflammatory programmed cell death. Caspase-1 is involved in various types of diseases, including hepatic injury, cancers, and diabetes-related complications. However, the exact role of caspase-1 in cardiac hypertrophy is yet to be discovered. The present study aimed to explore the possible role of caspase-1 in pathogenesis of cardiac hypertrophy. We established cardiac hypertrophy models both in vivo and in vitro to detect the expression of caspase-1 and interleukin-1β (IL-1β). The results showed that caspase-1 and IL-1β expression levels were significantly up-regulated during cardiac hypertrophy. Subsequently, caspase-1 inhibitor was co-administered with angiotensin II (Ang II) in cardiomyocytes to observe whether it could attenuate cardiac hypertrophy. Results showed that caspase-1 attenuated the pro-hypertrophic effect of Ang II, which was related to the down-regulation of caspase-1 and IL-1β. In conclusion, our results provide a novel evidence that caspase-1 mediated pyroptosis is involved in cardiac hypertrophy, and the inhibition of caspase-1 will offer a therapeutic potential against cardiac hypertrophy.