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Caffeic acid mitigates myocardial fibrosis and improves heart function in post-myocardial infarction by inhibiting transforming growth factor-ß receptor 1 signaling pathways.
Jiang, Weihao; Deng, Bo; Xie, Mengting; Feng, Yunting; Jiang, Xiaoli; Yang, Bo; Tan, Zhangbin; Ou, Hongbin; Tan, Yongzhen; Liu, Shaojun; Zhang, Shuangwei; Zhang, Jingzhi; Zhou, Yingchun; Wu, Weiwei; Liu, Bin.
Afiliação
  • Jiang W; Department of Traditional Chinese Medicine, Guangzhou Institute of Cardiovascular Disease, State Key Laboratory of Respiratory Disease, Institute of Integration of Traditional and Western Medicine of Guangzhou Medical University, The Second Affiliated Hospital of Guangzhou Medical University, No.250
  • Deng B; Department of Traditional Chinese Medicine, Guangzhou Institute of Cardiovascular Disease, State Key Laboratory of Respiratory Disease, Institute of Integration of Traditional and Western Medicine of Guangzhou Medical University, The Second Affiliated Hospital of Guangzhou Medical University, No.250
  • Xie M; Department of Traditional Chinese Medicine, Guangzhou Institute of Cardiovascular Disease, State Key Laboratory of Respiratory Disease, Institute of Integration of Traditional and Western Medicine of Guangzhou Medical University, The Second Affiliated Hospital of Guangzhou Medical University, No.250
  • Feng Y; Department of Traditional Chinese Medicine, Guangzhou Institute of Cardiovascular Disease, State Key Laboratory of Respiratory Disease, Institute of Integration of Traditional and Western Medicine of Guangzhou Medical University, The Second Affiliated Hospital of Guangzhou Medical University, No.250
  • Jiang X; Department of Traditional Chinese Medicine, Guangzhou Institute of Cardiovascular Disease, State Key Laboratory of Respiratory Disease, Institute of Integration of Traditional and Western Medicine of Guangzhou Medical University, The Second Affiliated Hospital of Guangzhou Medical University, No.250
  • Yang B; Department of Traditional Chinese Medicine, Guangzhou Institute of Cardiovascular Disease, State Key Laboratory of Respiratory Disease, Institute of Integration of Traditional and Western Medicine of Guangzhou Medical University, The Second Affiliated Hospital of Guangzhou Medical University, No.250
  • Tan Z; Department of Traditional Chinese Medicine, Guangzhou Institute of Cardiovascular Disease, State Key Laboratory of Respiratory Disease, Institute of Integration of Traditional and Western Medicine of Guangzhou Medical University, The Second Affiliated Hospital of Guangzhou Medical University, No.250
  • Ou H; Department of Traditional Chinese Medicine, Guangzhou Institute of Cardiovascular Disease, State Key Laboratory of Respiratory Disease, Institute of Integration of Traditional and Western Medicine of Guangzhou Medical University, The Second Affiliated Hospital of Guangzhou Medical University, No.250
  • Tan Y; Department of Traditional Chinese Medicine, Guangzhou Institute of Cardiovascular Disease, State Key Laboratory of Respiratory Disease, Institute of Integration of Traditional and Western Medicine of Guangzhou Medical University, The Second Affiliated Hospital of Guangzhou Medical University, No.250
  • Liu S; Guangzhou Institute of Cardiovascular Disease, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, China.
  • Zhang S; Department of Traditional Chinese Medicine, Guangzhou Institute of Cardiovascular Disease, State Key Laboratory of Respiratory Disease, Institute of Integration of Traditional and Western Medicine of Guangzhou Medical University, The Second Affiliated Hospital of Guangzhou Medical University, No.250
  • Zhang J; Department of Traditional Chinese Medicine, Guangzhou Institute of Cardiovascular Disease, State Key Laboratory of Respiratory Disease, Institute of Integration of Traditional and Western Medicine of Guangzhou Medical University, The Second Affiliated Hospital of Guangzhou Medical University, No.250
  • Zhou Y; School of Traditional Chinese Medicine, Department of Traditional Chinese Medicine, Nanfang Hospital (ZengCheng Branch), Southern Medical University, Guangzhou 510515, China. Electronic address: zhychun@126.com.
  • Wu W; Department of Rehabilitation, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, China. Electronic address: gyeywu@126.com.
  • Liu B; Department of Traditional Chinese Medicine, Guangzhou Institute of Cardiovascular Disease, State Key Laboratory of Respiratory Disease, Institute of Integration of Traditional and Western Medicine of Guangzhou Medical University, The Second Affiliated Hospital of Guangzhou Medical University, No.250
Biomed Pharmacother ; 177: 117012, 2024 Aug.
Article em En | MEDLINE | ID: mdl-38906025
ABSTRACT
Myocardial fibrosis is a pathological, physiological change that results from alterations, such as inflammation and metabolic dysfunction, after myocardial infarction (MI). Excessive fibrosis can cause cardiac dysfunction, ventricular remodeling, and heart failure. Caffeic acid (CA), a natural polyphenolic acid in various foods, has cardioprotective effects. This study aimed to explore whether CA exerts a cardioprotective effect to inhibit myocardial fibrosis post-MI and elucidate the underlying mechanisms. Histological observations indicated that CA ameliorated ventricular remodeling induced by left anterior descending coronary artery ligation in MI mice and partially restored cardiac function. CA selectively targeted transforming growth factor-ß receptor 1 (TGFBR1) and inhibited TGFBR1-Smad2/3 signaling, reducing collagen deposition in the infarcted area of MI mice hearts. Furthermore, cell counting (CCK-8) assay, 5-ethynyl-2'-deoxyuridine assay, and western blotting revealed that CA dose-dependently decreased the proliferation, collagen synthesis, and activation of the TGFBR1-Smad2/3 pathway in primary cardiac fibroblasts (CFs) stimulated by TGF-ß1 in vitro. Notably, TGFBR1 overexpression in CFs partially counteracted the inhibitory effects of CA. These findings suggest that CA effectively mitigates myocardial fibrosis and enhances cardiac function following MI and that this effect may be associated with the direct targeting of TGFBR1 by CA.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fibrose / Ácidos Cafeicos / Transdução de Sinais / Receptor do Fator de Crescimento Transformador beta Tipo I / Camundongos Endogâmicos C57BL / Infarto do Miocárdio / Miocárdio Limite: Animals Idioma: En Revista: Biomed Pharmacother Ano de publicação: 2024 Tipo de documento: Article
Texto completo
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XML
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fibrose / Ácidos Cafeicos / Transdução de Sinais / Receptor do Fator de Crescimento Transformador beta Tipo I / Camundongos Endogâmicos C57BL / Infarto do Miocárdio / Miocárdio Limite: Animals Idioma: En Revista: Biomed Pharmacother Ano de publicação: 2024 Tipo de documento: Article