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<p>Cardiac fibrosis, marked by excessive extracellular matrix accumulation, is a key endpoint in various cardiac diseases and is linked to energy metabolic disorders. This review explores the relationship between mitochondrial energy metabolism and cardiac fibrosis, focusing on the metabolic reprogramming in fibroblasts and cardiomyocytes during fibrosis development. We examine changes in substrate utilization, oxidative phosphorylation (OXPHOS), and ATP production that characterize the fibrotic heart. The metabolic dysregulation involves disruptions in fatty acid oxidation, glucose metabolism, and amino acid metabolism, contributing to fibrosis pathogenesis. Additionally, we discuss the implications of these metabolic alterations for therapeutic strategies, highlighting the potential of targeting energy metabolism to reverse or halt cardiac fibrosis progression. By synthesizing current knowledge and identifying research gaps, this review aims to lay the groundwork for future studies and enhance therapeutic approaches for this challenging condition.</p> Graphical Abstract <p></p>

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Reprogramming of Mitochondrial and Cellular Energy Metabolism in Fibroblasts and Cardiomyocytes: Mechanisms and Therapeutic Strategies in Cardiac Fibrosis

  • 期刊论文

  • 发表日期：

    2025年8月18日

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  • Junyan Zhang,
  • Yuting Lei,
  • Li Rao,
  • Yong He,
  • Zhongxiu Chen

摘要

Cardiac fibrosis, marked by excessive extracellular matrix accumulation, is a key endpoint in various cardiac diseases and is linked to energy metabolic disorders. This review explores the relationship between mitochondrial energy metabolism and cardiac fibrosis, focusing on the metabolic reprogramming in fibroblasts and cardiomyocytes during fibrosis development. We examine changes in substrate utilization, oxidative phosphorylation (OXPHOS), and ATP production that characterize the fibrotic heart. The metabolic dysregulation involves disruptions in fatty acid oxidation, glucose metabolism, and amino acid metabolism, contributing to fibrosis pathogenesis. Additionally, we discuss the implications of these metabolic alterations for therapeutic strategies, highlighting the potential of targeting energy metabolism to reverse or halt cardiac fibrosis progression. By synthesizing current knowledge and identifying research gaps, this review aims to lay the groundwork for future studies and enhance therapeutic approaches for this challenging condition.

Graphical Abstract