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CSN5 attenuates Ang II-induced cardiac hypertrophy through stabilizing LKB1
Zhiyong Sheng1, Yun Xu2, Fuxin Li1
1Intensive Care Unit, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Experimental Cell Research
|February 3, 2019
Summary
The COP9 signalosome subunit CSN5 protects against cardiac hypertrophy by stabilizing LKB1, a key regulator of AMP-activated protein kinase (AMPK). Activating the CSN5/LKB1 pathway may offer a novel treatment for hypertrophic cardiomyopathy.
Area of Science:
- Cardiology
- Molecular Biology
- Cell Biology
Background:
- The COP9 signalosome (CSN) subunit CSN5 plays roles in cellular processes, but its function in cardiac disease remains unclear.
- Cardiac hypertrophy is a significant risk factor for heart failure.
Purpose of the Study:
- To investigate the role of CSN5 in Angiotensin II (Ang II)-induced cardiac hypertrophy.
- To elucidate the molecular mechanism by which CSN5 affects cardiac hypertrophy.
Main Methods:
- Utilized Angiotensin II (Ang II) to induce cardiac hypertrophy in mouse models and cultured cardiomyocytes.
- Examined CSN5 expression levels and its effects on cardiac hypertrophy through overexpression and silencing.
- Investigated the interaction between CSN5 and LKB1, and its impact on AMP-activated protein kinase (AMPK) activity.
Main Results:
- CSN5 expression was upregulated in Ang II-induced cardiac hypertrophy.
- Overexpression of CSN5 inhibited Ang II-induced cardiac hypertrophy, while CSN5 silencing exacerbated it.
- CSN5 directly interacted with and deubiquitinated LKB1, enhancing its stability and maintaining AMPK activity.
Conclusions:
- CSN5 plays a protective role against cardiac hypertrophy by stabilizing LKB1 and activating the AMPK pathway.
- The CSN5/LKB1 axis represents a potential therapeutic target for hypertrophic cardiomyopathy.
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