Myocardial infarction (MI) often induces acute kidney injury (AKI) via systemic hypoperfusion and oxidative stress, yet the protective mechanisms of exercise remain unclear. This study investigated whether intermittent exercise alleviates MI-induced AKI through the insulin-like growth factor-1 (IGF-1)/PI3K/AKT signaling pathway. An AKI model was established in mice via coronary artery ligation, followed by moderate-intensity intermittent treadmill training for 4 weeks. Echocardiography, serum biochemical markers, renal histology, RT-qPCR, and Western blotting were used to assess cardiac and renal function, inflammatory cytokines, oxidative stress, apoptosis, and IGF-1/PI3K/AKT signaling. In vitro , H ₂ O ₂ -treated NRK renal cells were used to mimic oxidative damage. Recombinant human IGF-1 (rhIGF-1), AMPK agonist AICAR, IGF-1 receptor inhibitor NVP-AEW541, and PI3K inhibitor LY294002 were applied to explore the pathway’s involvement in exercise-induced renoprotection. MI led to impaired cardiac function, renal structural injury, elevated BUN and MDA levels, increased expression of IL-6, TNF-α, Bax, and Cleaved Caspase-3, and decreased SOD activity. Intermittent exercise improved cardiac output, attenuated renal injury, enhanced antioxidant capacity, and upregulated IGF-1 expression and its downstream PI3K/AKT signaling. In vitro , rhIGF-1 and AICAR mimicked the protective effects of exercise, while IGF-1R or PI3K inhibitors partially abolished these effects. These findings suggest that intermittent exercise ameliorates MI-induced AKI by activating the IGF-1/PI3K/AKT pathway, thereby exerting anti-inflammatory, antioxidant, and anti-apoptotic effects. This study highlights the role of exercise-induced IGF-1 in heart-kidney axis protection and provides a mechanistic basis for therapeutic interventions targeting MI-related renal complications.

Regular exercise and physical activity are beneficial in reducing the risk and progression of ischemic stroke. However, the underlying physiological mechanisms by which exercise confers these protective effects remain incompletely understood. Disruption of mitochondrial homeostasis is key contributors to the pathophysiology of ischemic stroke. Exercise training effectively attenuates the onset and progression of ischemic stroke by significantly maintaining mitochondrial homeostasis, including improving mitochondrial biogenesis, balancing mitochondrial dynamics, maintaining mitochondrial redox, promoting mitophagy and mitochondrial transport. This review systematically summarizes the beneficial effects of exercise in the context of ischemic stroke and highlights the critical link between mitochondrial homeostasis disruption and stroke pathology. By providing a detailed analysis of the underlying molecular mechanisms, this study offers novel insights into exercise-based therapeutic strategies for ischemic stroke.

Exercise is one of the safe and effective methods to improve obesity and its complications, but the mechanism has not been fully elucidated. Sestrin2 (SESN2) is a stress-induced protein that protects cells from stress damage. The role and mechanism of SESN2 in the improvement of obesity-induced cardiac dysfunction by exercise are still unclear. Male C57BL/6J mice were used to prepare a high-fat diet-induced obesity mouse model and conducted aerobic exercise training. After training, echocardiography was used to evaluate the cardiac function of mice, and HE and Masson staining were used to assess the extent of cardiac damage. Cell experiments were conducted using the H9C2 cell line derived from embryonic rat hearts, with the intervention of palmitic acid ester and exogenous SESN2. We detected indicators related to myocardial cell damage, fibrosis, inflammation, and oxidative stress, as well as the activation level of the AMPK-PGC-1α signaling pathway. The results showed that aerobic exercise significantly inhibited myocardial fibrosis, inflammation, oxidative stress, and cell damage in HFD mice, upregulated cardiac SESN2 expression, and activated the AMPK-PGC-1α signaling pathway. Cell experiments have found that exogenous SESN2 pretreatment alleviates palmitate-induced injury, inflammation, and oxidative stress in H9C2 cardiomyocytes, and activates the AMPK-PGC-1α signaling pathway. This indicates that aerobic exercise significantly upregulates the expression of SESN2 and activates the AMPK-PGC-1α signaling pathway, which is potentially involved in alleviating myocardial inflammation, oxidative stress, cardiac fibrosis and cardiac dysfunction in HFD mice.