Rehabilitation exercise ameliorated aging myocardial injury and improved cardiac function in rats by suppressing the ILK/Integrin β3αv/p38 MAPK pathway (P<0.05 for reduced apoptosis and senescence).
Does rehabilitation exercise improve aging myocardial injury in a D-galactose-induced rat model?
Rehabilitation exercise ameliorates aging-induced myocardial injury and improves cardiac function in rats by suppressing the ILK/Integrin β3αv/p38 MAPK signaling pathway.
p-value: p=<0.05
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.
欧东波 et al. (Tue,) conducted a other in Aging myocardial injury. Rehabilitation exercise vs. Model group (no exercise) was evaluated on Myocardial damage, senescence, apoptosis, and cardiac function (p=<0.05). Rehabilitation exercise ameliorated aging myocardial injury and improved cardiac function in rats by suppressing the ILK/Integrin β3αv/p38 MAPK pathway (P<0.05 for reduced apoptosis and senescence).