Rehabilitation exercise improves aging myocardial injury by suppressing the ILK/integrin β3αv/p38 MAPK signaling pathway

OBJECTIVE: This study investigated whether rehabilitation exercise improves aging myocardial injury by modulating the ILK/Integrin β3αv/p38 MAPK pathway, and examined how ILK overexpression affects cardiomyocyte senescence and apoptosis. METHODS: A rat aging model was induced by D-galactose. Rats underwent rehabilitation training. Myocardial pathology and mitochondrial structure were observed. Protein expression (P21, P53, γH2AX) was measured by Western blot, and apoptosis by TUNEL staining. Post-intervention cardiac function was assessed by echocardiography. RESULTS: 1) The exercise group showed reduced myocardial damage, improved fiber arrangement, less inflammation, and recovered mitochondrial ultrastructure. 2) SASP factors (IL-6, IL-13, MCP-2, MCP-3) were lower vs. model group (P < 0.05). SA-β-gal-positive cells and apoptosis decreased (P < 0.05), while P21, P53, and γH2AX expression were reduced (P < 0.01). Telomere length increased (P < 0.05). 3) ILK, Integrin β3αv, and p-p38 MAPK/t-p38 MAPK ratio were downregulated after exercise (P < 0.01). 4) ILK overexpression blunted the benefits of exercise, with the model + treadmill + OE-ILK group showing the most severe injury. 5) Echocardiography revealed that exercise improved left ventricular ejection fraction (LVEF) and fractional shortening (FS), effects reversed by ILK overexpression. CONCLUSION: Rehabilitation exercise ameliorated aging myocardial injury by suppressing the ILK/Integrin β3αv/p38 MAPK pathway, an effect reversed by ILK overexpression.