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Mitochondria, commonly referred to as "energy factories"of cells, play a crucial role in the function and survival of cardiomyocytes. However, as research on cardiac fibrosis has advanced, mitochondrial dysfunction(including changes in energy metabolism, calcium ion imbalance, increased oxidative stress, and apoptosis)is now recognized as a significant pathophysiological pathway involved in cardiac remodeling and progression, which also negatively affects the function and structure of the heart. In recent years, research focusing on targeting mitochondria has gained significant attention, offering new approaches for treating cardiac fibrosis. Targeted mitochondrial therapy for cardiac fibrosis represents an emerging therapeutic strategy that aims to inhibit cardiac fibroblast proliferation or protect cardiomyocytes from damage by enhancing mitochondrial function. However, current research on epigenetic treatments for cardiac fibrosis through mitochondrial targeting remains limited. This review explores the relationship between mitochondrial dysfunction and cardiac fibrosis, as well as the epigenetic regulatory mechanisms involved in targeted mitochondrial therapy for cardiac fibrosis., Competing Interests: Declaration of competing interest None., (Copyright © 2025 Elsevier Inc. All rights reserved.)