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Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

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Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...

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Related Experiment Video

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YTHDF3-mediated FLCN/cPLA2 axis improves cardiac fibrosis via suppressing lysosomal function.

Yue Zhang1, Hong-Tao Diao1, Ming-Yang Leng1

  • 1Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China, Guangdong Key Laboratory of Metabolic Disease Prevention and Treatment of Traditional Chinese Medicine, Key Unit of Modulating Liver to Treat Hyperlipemia SATCM, State Administration of Traditional Chinese Medicine, Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, 510006, China.

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Folliculin (FLCN) inhibits cardiac fibrosis by regulating lysosomal function and interacting with cPLA2. FLCN

Keywords:
FLCNYTHDF3cPLA2cardiac fibrosislysosomem6A

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Area of Science:

  • Cardiovascular Biology
  • Fibrosis Research
  • Molecular Mechanisms of Disease

Background:

  • Cardiac fibrosis, driven by fibroblast activation, impairs heart function and leads to heart failure.
  • Folliculin (FLCN), known for roles in cellular processes, has been linked to severe heart failure in knockout models.
  • Inhibition of cardiac fibrosis is a key therapeutic strategy for cardiac diseases.

Purpose of the Study:

  • To investigate the role of Folliculin (FLCN) in cardiac fibrosis.
  • To elucidate the underlying mechanisms of FLCN's action in cardiac fibroblasts.
  • To explore FLCN and YTHDF3 as potential therapeutic targets for myocardial fibrosis.

Main Methods:

  • Transverse aortic constriction (TAC) surgery in mice to induce cardiac fibrosis.
  • In vitro studies using primary mouse cardiac fibroblasts treated with Ang-II.
  • Analysis of FLCN protein and mRNA expression levels.
  • Investigation of FLCN's interaction with cPLA2 and its effect on lysosomal function.
  • Assessment of YTHDF3's role in FLCN mRNA methylation and its impact on cardiac fibrosis.

Main Results:

  • FLCN expression was significantly decreased in TAC mice and Ang-II treated fibroblasts.
  • FLCN overexpression inhibited lysosomal function and protected against TAC-induced cardiac fibrosis.
  • FLCN interacted with cPLA2, enhancing its activity and improving lysosomal function.
  • Reduced FLCN expression was linked to YTHDF3-regulated m6A methylation of FLCN mRNA.
  • YTHDF3 overexpression alleviated fibrosis, improved cardiac structure and function in TAC mice.

Conclusions:

  • FLCN plays a protective role against cardiac fibrosis by regulating lysosomal function and interacting with cPLA2.
  • YTHDF3-mediated m6A modification of FLCN mRNA influences its expression and contributes to cardiac fibrosis.
  • FLCN and YTHDF3 represent potential therapeutic targets for treating cardiac fibroblast-mediated myocardial fibrosis.