Aerobic exercise modulates macrophage polarization and promotes cardiac recovery after myocardial infarction in rats.
6 affiliations
- 1Department of Cardiovascular Medicine, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
- 2Department of Obstetrics, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
- 3Department of Clinical Laboratory, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
- 4Department of Medical Ultrasonics, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
- 5Department of Medical Ultrasonics, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China. [email protected].
- 6The Second Affiliated Hospital, Hengyang Medical School, University of South China, No. 35 Jiefang Avenue, Zhengxiang District, Hengyang City, Hunan Province, China. [email protected].
Abstract
Objective
To evaluate the protective effects of aerobic exercise (AE) on cardiac function and myocardial injury in rats with myocardial infarction (MI), as well as its impact on macrophage polarization.Methods
A rat model of chronic post-infarction remodeling was established by ligation of the left anterior descending coronary artery, while the Sham group underwent threading without ligation. After a 4-week recovery period, rats in the exercise group underwent an 8-week aerobic training program, with all assessments performed at approximately 12 weeks after MI induction. The maximal aerobic velocity test was performed to assess changes in exercise endurance. To evaluate cardiac architecture, inflammatory infiltrates, and the extent of fibrosis, we performed standard histological staining with hematoxylin-eosin and Masson's trichrome. Triphenyltetrazolium chloride staining was applied to distinguish infarcted and viable myocardial regions. Commercial assay kits were used to detect myocardial injury markers, inflammatory cytokines, and oxidative stress indicators in myocardial tissue or serum. Western blotting and immunofluorescence staining were performed to assess macrophage polarization.Results
AE markedly improved cardiac function in MI rats. It also attenuated MI size and fibrosis. Serum levels of cardiac damage-associated biomarkers (cTnI, CK-MB, and LDH) were significantly decreased following AE, suggesting attenuation of ongoing myocardial injury and adverse remodeling in the chronic post-infarction setting, as were pro-inflammatory cytokines and oxidative stress indicators. Anti-inflammatory and antioxidant capacity were also enhanced by AE. M1 macrophage markers were reduced, along with upregulation of M2 macrophage markers in the myocardial tissue after AE.Conclusion
Moderate-intensity AE alleviates myocardial injury, inflammation, and oxidative stress, and promotes macrophage polarization toward the M2 phenotype in rats with MI. These findings may provide evidence for exercise-based rehabilitation and immune-targeted therapeutic strategies.
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BibTeX
@article{zhu2026aerobic,
title = {{Aerobic exercise modulates macrophage polarization and promotes cardiac recovery after myocardial infarction in rats.}},
author = {Mingyan Zhu and Bing Zhou and Jianye Peng and Kong Chen and Yu Wang and Hao Zeng and Xia Zhang},
journal = {Journal of cardiothoracic surgery},
year = {2026},
month = jul,
doi = {10.1186/s13019-026-04603-x},
url = {https://europepmc.org/article/MED/42902400},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Aerobic exercise modulates macrophage polarization and promotes cardiac recovery after myocardial infarction in rats.
AU - Mingyan Zhu
AU - Bing Zhou
AU - Jianye Peng
AU - Kong Chen
AU - Yu Wang
AU - Hao Zeng
AU - Xia Zhang
PY - 2026
DA - 2026/07/01
JO - Journal of cardiothoracic surgery
DO - 10.1186/s13019-026-04603-x
UR - https://europepmc.org/article/MED/42902400
AB - Objective To evaluate the protective effects of aerobic exercise (AE) on cardiac function and myocardial injury in rats with myocardial infarction (MI), as well as its impact on macrophage polarization.Methods A rat model of chronic post-infarction remodeling was established by ligation of the left anterior descending coronary artery, while the Sham group underwent threading without ligation. After a 4-week recovery period, rats in the exercise group underwent an 8-week aerobic training program, with all assessments performed at approximately 12 weeks after MI induction. The maximal aerobic velocity test was performed to assess changes in exercise endurance. To evaluate cardiac architecture, inflammatory infiltrates, and the extent of fibrosis, we performed standard histological staining with hematoxylin-eosin and Masson's trichrome. Triphenyltetrazolium chloride staining was applied to distinguish infarcted and viable myocardial regions. Commercial assay kits were used to detect myocardial injury markers, inflammatory cytokines, and oxidative stress indicators in myocardial tissue or serum. Western blotting and immunofluorescence staining were performed to assess macrophage polarization.Results AE markedly improved cardiac function in MI rats. It also attenuated MI size and fibrosis. Serum levels of cardiac damage-associated biomarkers (cTnI, CK-MB, and LDH) were significantly decreased following AE, suggesting attenuation of ongoing myocardial injury and adverse remodeling in the chronic post-infarction setting, as were pro-inflammatory cytokines and oxidative stress indicators. Anti-inflammatory and antioxidant capacity were also enhanced by AE. M1 macrophage markers were reduced, along with upregulation of M2 macrophage markers in the myocardial tissue after AE.Conclusion Moderate-intensity AE alleviates myocardial injury, inflammation, and oxidative stress, and promotes macrophage polarization toward the M2 phenotype in rats with MI. These findings may provide evidence for exercise-based rehabilitation and immune-targeted therapeutic strategies.
SN - 1749-8090
ER -