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Figure 5. Alterations in mitonuclear communication during cardiac aging. In young cardiomyocytes, mitonuclear signaling - mediated by the coactivators PGC-1α and PGC-1β and the transcription factor KLF15 - supports mitochondrial biogenesis, oxidative metabolism, and cellular homeostasis. In contrast, aged cardiomyocytes exhibit disrupted mitonuclear communication, characterized by downregulation of PGC-1α/β and a shift toward Klf5 expression. This imbalance contributes to mitochondrial dysfunction, increased production of reactive oxygen species (ROS), cellular senescence, and pathological hypertrophy, ultimately promoting adverse cardiac remodeling and age-related functional decline.