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Biosci Rep. 2018 Feb 12. pii: BSR20171438. doi: 10.1042/BSR20171438. [Epub ahead of print]

Caspase-1 regulate AngII-induced cardiomyocyte hypertrophy via upregulation of IL-1β.

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Pharmacology, Harbin Medical University, Harbin, China
Pharmacology, Harbin Medical University, Harbin, China.
Chronic Disease Research Institute, Harbin Medical University, Harbin, China.
Translational Medicine Research and Cooperation Center of Northern China, Harbin, China.


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 IL-1β. The results showed that caspase-1 and IL-1β expression levels were significantly upregulated 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 downregulation 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.


Cardiac hypertrophy; IL-1β; caspase-1; pyroptosis

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