Scholarlink

<p>Hypertrophic cardiomyopathy (HCM) is characterized by cardiac hypertrophy and fibrosis. To investigate the impact of CARMA3 on fibroblast phenotypic transformation in hypertrophic cardiomyopathy (HCM), the correlation between CARMA3 expression and fibrosis was analyzed in HCM patients. Cardiac function and fibroblast phenotypic transformation were assessed in wild-type and CARMA3-knockout mice subjected to transverse aortic constriction (TAC) or angiotensin II treatment. Additionally, cardiac fibroblasts were screened using flow cytometry and proteomic analysis to identify potential targets. Significant cardiac functional impairment and fibrosis were observed in CARMA3-knockout mice following TAC or angiotensin II treatment. Primary fibroblasts isolated from these mice exhibited increased myofibroblast differentiation, extracellular collagen production, mitochondrial damage, and macrophage inflammation. Elevated STAT1 expression was identified in cardiac fibroblasts from CARMA3-knockout mice through proteomic analysis. Additionally, STAT1 phosphorylation was regulated by CARMA3, and an interaction between CARMA3 and STAT1 was detected in response to pressure overload. In conclusion, CARMA3 may suppress myofibroblast activation by inhibiting STAT1 phosphorylation, thereby improving myocardial fibrosis in pressure overload-induced HCM.</p><p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

The role of CARMA3 in regulating fibrosis to prevent hypertrophic cardiomyopathy

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月6日

查看全文
  • Yafeng Liu,
  • Ganyi Chen,
  • Yiwei Yao,
  • Yunfei Jiang,
  • Chenghao Wen,
  • Wuwei Wang,
  • Quan Liu,
  • Yide Cao,
  • Fuhua Huang,
  • Wen Chen,
  • Zhibing Qiu

摘要

Hypertrophic cardiomyopathy (HCM) is characterized by cardiac hypertrophy and fibrosis. To investigate the impact of CARMA3 on fibroblast phenotypic transformation in hypertrophic cardiomyopathy (HCM), the correlation between CARMA3 expression and fibrosis was analyzed in HCM patients. Cardiac function and fibroblast phenotypic transformation were assessed in wild-type and CARMA3-knockout mice subjected to transverse aortic constriction (TAC) or angiotensin II treatment. Additionally, cardiac fibroblasts were screened using flow cytometry and proteomic analysis to identify potential targets. Significant cardiac functional impairment and fibrosis were observed in CARMA3-knockout mice following TAC or angiotensin II treatment. Primary fibroblasts isolated from these mice exhibited increased myofibroblast differentiation, extracellular collagen production, mitochondrial damage, and macrophage inflammation. Elevated STAT1 expression was identified in cardiac fibroblasts from CARMA3-knockout mice through proteomic analysis. Additionally, STAT1 phosphorylation was regulated by CARMA3, and an interaction between CARMA3 and STAT1 was detected in response to pressure overload. In conclusion, CARMA3 may suppress myofibroblast activation by inhibiting STAT1 phosphorylation, thereby improving myocardial fibrosis in pressure overload-induced HCM.