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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

Miaomiao Yang   *
1   Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China
2   Tianjin Key Lab of Exercise Physiology and Sports Medicine, Tianjin University of Sport, Tianjin 301617, China
,
Zhigang Xiao   *
1   Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China
3   School of Materials Science and Engineering,Tianjin University of Technology, Tianjin 300384, China
,
Zhaoli Chen   *
1   Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China
,
Yongxin Ru
4   Institute of Hematology and Blood Diseases Hospital Peaking Union Medical College, Tianjin 300020, China
,
Jun Wang
5   Air Force Medical Center, Medical Evaluation Department, Beijing 100042, China
,
Jianhua Jiang
1   Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China
,
Xinxing Wang 
1   Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China
,
Tianhui Wang
1   Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China
2   Tianjin Key Lab of Exercise Physiology and Sports Medicine, Tianjin University of Sport, Tianjin 301617, China
› Author Affiliations Funding This work was partially supported by the grants of the Natural Science Foundation of China [grant numbers 81373108, 31971106, 17-163-12-ZT-002-120-01, 18CXZ044].
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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

* These authors contributed equally to this work.




Publication History

Received: 12 July 2020

Accepted: 08 September 2021

Article published online:
23 October 2021

© 2021. Thieme. All rights reserved.

Georg Thieme Verlag KG
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