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Updated: Jun 7, 2025

In Vitro Assessment of Cardiac Function Using Skinned Cardiomyocytes
Published on: June 22, 2020
Myoferlin alleviates pressure overload-induced cardiac hypertrophy and dysfunction by inhibiting NLRP3-mediated
Yang Zhou1, Yanxu Liu1, Hao Luo1
1Department of Cardiology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, China.
Abstract:
Myoferlin (MYOF) is a muscle-derived secretory protein. Recent studies have found that MYOF protects against cell damage. However, the role of MYOF in cardiac hypertrophy remains unclear. Increasing evidence suggests that NLRP3 (NOD-like receptor protein 3) and the pyroptosis cascade play critical roles in the development of cardiac hypertrophy and inflammation. To investigate the role of MYOF in cardiac hypertrophy, we conducted a transverse aortic constriction (TAC) experiment in a mouse model. We found that MYOF can improve cardiac hypertrophy and cardiac function. Furthermore, our study confirmed a connection between cardiac hypertrophy and myocardial pyroptosis. Cardiac hypertrophy significantly increased the proportion of apoptotic cells and upregulated apoptosis-associated speck-like protein containing a CARD (ASC), caspase-1, and gasdermin D (GSDMD). This suggests that pharmacological or genetic inhibition of NLRP3 can effectively reduce cardiac hypertrophy. An abnormal increase in NLRP3 can reverse the cardioprotective effects of MYOF. Our findings indicate that MYOF is a potential therapeutic agent for cardiac hypertrophy.
Insights
Myoferlin (MYOF) protein protects against cardiac hypertrophy and improves heart function. Inhibiting NLRP3 inflammation pathways enhances MYOF
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Inflammation Research
Background:
- Myoferlin (MYOF) is a muscle-derived secretory protein with known protective functions against cell damage.
- The role of MYOF in cardiac hypertrophy, a condition of heart muscle thickening, is not well understood.
- NLRP3 inflammasome and pyroptosis are implicated in cardiac hypertrophy and inflammation.
Purpose of the Study:
- To investigate the role of Myoferlin (MYOF) in the context of cardiac hypertrophy.
- To explore the relationship between MYOF, cardiac hypertrophy, and the pyroptosis pathway.
- To assess the therapeutic potential of MYOF for cardiac hypertrophy.
Main Methods:
- A mouse model of cardiac hypertrophy was established using transverse aortic constriction (TAC).
- MYOF expression and its effects on cardiac function and hypertrophy were analyzed.
- The expression of pyroptosis markers, including ASC, caspase-1, and GSDMD, was evaluated.
Main Results:
- Myoferlin (MYOF) administration improved cardiac hypertrophy and cardiac function in the TAC model.
- Cardiac hypertrophy was associated with increased myocardial pyroptosis, evidenced by elevated ASC, caspase-1, and GSDMD.
- Abnormal NLRP3 (NOD-like receptor protein 3) activation reversed the cardioprotective effects of MYOF.
Conclusions:
- Myoferlin (MYOF) demonstrates significant cardioprotective effects against cardiac hypertrophy.
- The study confirms a link between cardiac hypertrophy, pyroptosis, and the NLRP3 inflammasome.
- MYOF presents a potential therapeutic strategy for treating cardiac hypertrophy.
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