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Research shows mitochondrial dysfunction affects cardiac health in aging, suggesting TPP may provide targeted intervention.
Aging leads to changes in many biological processes and their disruption leads to ailments. Understanding molecular mechanisms underpinning cardiac aging, with a prime focus on the contribution of dysfunctional mitochondria in this process is crucial. Mitochondrial dysfunction has been correlated to multiple cardiac diseases therefore, treating the mitochondria has helped in alleviating/preventing these conditions. It has also been observed that antioxidant moieties scavenge the excess ROS in the mitochondria and have significantly demonstrated a protective effect on mitochondria. The antioxidants however due to their molecular weight and their composition may or may not accumulate inside the cell and mitochondria. Targeting the mitochondria requires special modification and TPP is one such moiety. TPP facilitates the sequestered accumulation of the tagged compound inside mitochondria. Accumulating evidence from several in vitro and in vivo experimental models has proven the efficacy of this approach in ameliorating age-related cardiac impairments. These findings underscore the significance of mitochondrial health in the context of cardiac aging and provide a foundation for the development of targeted interventions aimed at preserving cardiac function during the aging process.
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Jaiswal et al. (2025) studied this question.
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