S100A1 is Involved in Myocardial Injury Induced by Exhaustive
                    Exercise

Miaomiao Yang; Zhigang Xiao; Zhaoli Chen; Yongxin Ru; Jun Wang; Jianhua Jiang; Xinxing Wang; Tianhui Wang

doi:10.1055/a-1642-8352

International Journal of Sports Medicine, Table of Contents

Int J Sports Med 2022; 43(05): 444-454
DOI: 10.1055/a-1642-8352

Genetics and Molecular Biology

S100A1 is Involved in Myocardial Injury Induced by Exhaustive Exercise

Authors

Miaomiao Yang^*

¹Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China

²Tianjin Key Lab of Exercise Physiology and Sports Medicine, Tianjin University of Sport, Tianjin 301617, China
Zhigang Xiao^*

¹Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China

³School of Materials Science and Engineering,Tianjin University of Technology, Tianjin 300384, China
Zhaoli Chen^*

¹Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China
Yongxin Ru

⁴Institute of Hematology and Blood Diseases Hospital Peaking Union Medical College, Tianjin 300020, China
Jun Wang

⁵Air Force Medical Center, Medical Evaluation Department, Beijing 100042, China
Jianhua Jiang

¹Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China
Xinxing Wang

¹Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China
Tianhui Wang

¹Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China

²Tianjin Key Lab of Exercise Physiology and Sports Medicine, Tianjin University of Sport, Tianjin 301617, China

Abstract

Many studies have confirmed that exhaustive exercise has adverse effects on the heart by generating reactive oxygen species (ROS). S100A1 calcium-binding protein A1 (S100A1) is a regulator of myocardial contractility and a protector against myocardial injury. However, few studies have investigated the role of S100A1 in the regulation of myocardial injury induced by exhaustive exercise. In the present study, we suggested that exhaustive exercise led to increased ROS, downregulation of S100a1, and myocardial injury. Downregulation of S100a1 promoted exhaustive exercise-induced myocardial injury and overexpression of S100A1 reversed oxidative stress-induced cardiomyocyte injury, indicating S100A1 is a protective factor against myocardial injury caused by exhaustive exercise. We also found that downregulation of S100A1 promoted damage to critical proteins of the mitochondria by inhibiting the expression of Ant1, Pgc1a, and Tfam under exhaustive exercise. Our study indicated S100A1 as a potential prognostic biomarker or therapeutic target to improve the myocardial damage induced by exhaustive exercise and provided new insights into the molecular mechanisms underlying the myocardial injury effect of exhaustive exercise.

Key words

oxidative stress - exhaustive exercise - mitochondrion

Full Text

References

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