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Figure 1. Age-related cellular, structural and functional maladaptation in the heart. Aging causes cardiomyocyte hypertrophy and senescence, leading to an accumulation of senescent cells that secrete pro-inflammatory factors known as the senescence-associated secretory phenotype (SASP). This triggers macrophage and granulocyte recruitment and myofibroblast activation in the heart. Mitochondrial dysfunction also occurs, reducing ATP production and increasing ROS, which contributes to endothelial cell dysfunction. These cellular impairments result in structural changes like pathological cardiac hypertrophy, increased myocardial stiffness, fibrosis, and vascular dysfunction, ultimately manifesting as diastolic dysfunction and diminished exercise tolerance.