Key result
Natural compounds and electroacupuncture reduce mitochondrial fission in preclinical MI/RI models, lacking clinical proof.
Why the study?
Myocardial ischemia/reperfusion injury remains an unresolved problem despite reperfusion therapies such as PCI, with excessive mitochondrial fission implicated in cardiomyocyte injury. Preclinical evidence for plant-derived interventions and electroacupuncture targeting this fission-dominant imbalance is limited by model heterogeneity, reliance on surrogate models, and unestablished clinical efficacy and safety.
Do plant-derived natural products, multi-component botanical preparations, and electroacupuncture modulate excessive mitochondrial fission and protect against myocardial ischemia/reperfusion injury in preclinical models?
Do plant-derived natural products, multi-component botanical preparations, and electroacupuncture modulate excessive mitochondrial fission and protect against myocardial ischemia/reperfusion injury in preclinical models?
This narrative review synthesizes preclinical evidence indicating that plant-derived interventions and electroacupuncture may mitigate myocardial ischemia/reperfusion injury by counteracting Drp1-mediated excessive mitochondrial fission and restoring fusion-fission balance, while highlighting major translational gaps.
Answers are grounded in this paper and cite their sources.
Clinical adoption in MI/RI remains premature; leaves open whether Drp1 modulation improves outcomes in trials.
Myocardial ischemia/reperfusion injury (MI/RI) remains an unresolved problem despite reperfusion therapies, including percutaneous coronary intervention. Mitochondria are central mediators of reperfusion-associated cardiomyocyte injury, with excessive fission implicated as a potentially important mechanism linking acute metabolic stress to fragmentation, bioenergetic failure, and cell death. Reactive oxygen species, Ca2+ overload, mitochondrial permeability transition pore opening and membrane-potential loss promote dynamin-related protein 1-centered (Drp1-centered) fission, often involving mitochondrial fission factor, mitochondrial fission 1 protein and site-specific Drp1 phosphorylation. By disrupting mitochondrial networks and oxidative phosphorylation, this process contributes to cytochrome c release, apoptosis, microvascular dysfunction and impaired recovery. Impaired mitofusin 1/2-mediated and optic atrophy 1-mediated fusion limits repair and quality control, supporting investigation of this fission-dominant imbalance as a target for cardioprotection. Preclinical studies suggest plant-derived natural products, multi-component botanical preparations and electroacupuncture may influence this imbalance. Reported effects include attenuated Drp1 signaling, altered fusion-protein expression, preserved membrane potential, inhibited permeability transition, reduced oxidative stress and apoptosis, and modulated upstream metabolic/stress-responsive pathways. However, hypoxia/reoxygenation, oxygen-glucose deprivation/reoxygenation, non-reperfused ischemia/infarction and stress models provide surrogate or supportive evidence rather than direct evidence of MI/RI. Heterogeneity in models, timing, dosage, readouts, causal validation and botanical quality control limits interpretation. This review examines these mechanisms, interventions and translational priorities. Clinical efficacy and safety of these interventions in MI/RI have not been established.
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Sun et al. (2026) conducted a review in Myocardial ischemia/reperfusion injury. Plant-derived natural products, multi-component botanical preparations, and electroacupuncture vs. Untreated or vehicle-treated ischemia/reperfusion control models was evaluated on Modulation of dynamin-related protein 1 (Drp1)-centered mitochondrial fission and fusion-fission balance in myocardial ischemia/reperfusion injury. Plant-derived interventions and electroacupuncture attenuate Drp1-mediated mitochondrial fission and preserve fusion in preclinical MI/RI models, though clinical efficacy remains unestablished.
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