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.

Peerj
|November 18, 2024
PubMed

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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