A review of mitochondrial dynamics finds that imbalance between fusion and fission is a shared feature of Alzheimer's disease, Parkinson's disease, cerebral infarction, atherosclerosis, myocardial infarction, hypertension, and cardiomyopathy. Because cardiac and neural tissue depend on uninterrupted energy supply, loss of mitochondrial plasticity translates directly into functional decline. Aerobic interval and treadmill training, metformin, dapagliflozin, irbesartan, and several traditional Chinese medicine compounds have shown capacity to restore that balance.
Key Points
- Fission-fusion imbalance underlies both neurodegenerative and cardiovascular aging disease
- Heart and brain tissue are most vulnerable to mitochondrial energy failure
- Aerobic interval training and metformin restore mitochondrial dynamic balance
Longevity Analysis
Cardiac and cerebral decline converge on the same upstream defect: mitochondria that can no longer divide, merge, and clear damaged copies on schedule. Interventions that restore this plasticity are largely ones already available — structured aerobic work, specific metabolic and antihypertensive agents — which shifts the question from discovery to disciplined application. Tracking cardiorespiratory capacity and metabolic markers over years, rather than single measurements, offers a practical read on whether energy-producing machinery in the tissues least tolerant of failure is holding its ground.
Original published by Wiley Aging Cell, by Yuyao Yin, Zijian Li .