Key result
Traditional Chinese Medicine attenuates myocardial fibrosis by restoring mitochondrial quality control balance.
Why the study?
Myocardial fibrosis leads to end-stage heart disease and effective reversal strategies are urgently needed, with mitochondrial quality control emerging as a key regulatory mechanism.
Systematic Review
This systematic review highlights the multi-target mechanisms of Traditional Chinese Medicine in mitigating myocardial fibrosis through the modulation of mitochondrial quality control.
Answers are grounded in this paper and cite their sources.
Should not yet change practice for myocardial fibrosis; leaves open mechanistic hypotheses for randomized trials.
Myocardial fibrosis (MF), characterized by excessive collagen deposition, represents an inevitable pathological progression toward end-stage heart disease, underscoring the urgent clinical need for effective reversal strategies. In recent years, the mitochondrial quality control (MQC) system has emerged as a central regulatory hub for maintaining cardiac homeostasis, offering novel insights into the prevention and treatment of MF. This review bridges classical Traditional Chinese Medicine (TCM) therapeutic concepts with modern MQC mechanisms, primarily aiming to evaluate the intervention targets and efficacy of TCM monomers and formulas by detecting alterations in mitochondrial-associated protein expression, gene transcription levels, and organelle ultrastructure. By systematically reviewing experimental evidence of TCM-mediated MQC modulation, this paper highlights the multi-target and systematic advantages of TCM in combating MF, thereby injecting new momentum into the development of contemporary anti-MF therapeutics.
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Li et al. (2026) conducted a systematic review in Myocardial fibrosis. Traditional Chinese Medicine monomers and formulas was evaluated. Traditional Chinese Medicine monomers and formulas ameliorate myocardial fibrosis by restoring the dynamic balance of mitochondrial quality control, including biogenesis, dynamics, autophagy, and proteostasis.
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