Molecular insights into mitoepigenetic stress response signaling in age-associated cardiovascular disease risk

Cardiovascular diseases (CVD) represent a major challenge for the elderly population and continue to be among the leading causes of mortality worldwide. The integrity of mitochondria in peripheral lymphocytes can indicate age-related degenerative disorders, revealing the balance between bioenergetics, inflammation, and senescence. The present study aims to investigate the impact of aging on mitochondrial-mediated epigenetic stress response mechanisms in both young and elderly individuals. Mitochondrial oxidative DNA damage, repair response, copy number, methylation, fusion, fission genes, electron transport chain enzyme complex activities, pro-inflammatory cytokine levels, and associated epigenetic mechanisms were studied. The results demonstrate that the elderly group experienced more significant disruption in the expression of mitochondrial genes, leading to impaired mitochondrial DNA (mtDNA) integrity intricately linked to mitochondrial-nuclear crosstalk, increasing their susceptibility to CVD. The findings highlight mitochondria’s crucial role in cellular dynamics, influencing stress responses and epigenetic mechanisms through fusion and fission cycles. Overall, these insights provide valuable information about the complex molecular processes linking mitochondrial dysfunction to age-related cardiovascular risks, paving the way for further exploration and potential interventions in aging-related health outcomes. Graphical Abstract Figure showing the molecular mechanisms underlying the mitoepigenetic stress response signaling pathways in age-associated cardiovascular diseases.