Strategic targeting of mitochondria in ischemic heart disease: mechanisms and emerging therapies.
Targeting mitochondria to treat heart damage from reduced blood flow: how it works and new treatments
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Abstract
Mitochondrial dysfunction is central to ischemia-reperfusion injury in ischemic heart disease (IHD).
- Mitochondrial dysfunction is associated with bioenergetic failure, oxidative stress, calcium overload, and impaired adaptive responses in IHD.
- Key pathways linked to mitochondrial dysfunction include reactive oxygen species generation, mitochondrial permeability transition pore activation, disrupted fusion-fission dynamics, mitophagy imbalance, and proteostasis collapse.
- Emerging therapeutic strategies may include mitochondria-targeted antioxidants, cardiolipin-stabilizing peptides, metabolic modulators, mitochondrial transplantation, and genome-directed approaches.
- Innovations in diagnostics may involve circulating mitochondrial DNA, mitomiRs, and molecular imaging.
- Precision targeting of mitochondrial injury and adaptive failure could provide stage-specific therapeutic opportunities in IHD.
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