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S100A8/A9 in Myocardial Infarction: A Promising Biomarker and Therapeutic Target
ZhuLan Cai1,2, Qingwen Xie1,2, Tongtong Hu1,2
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Insights
S100A8/A9 alarmins play a key role in myocardial infarction (MI) pathogenesis by influencing inflammation and repair. Understanding these roles may reveal new therapeutic targets for heart attack treatment.
Area of Science:
- Cardiology
- Immunology
- Biochemistry
Background:
- Myocardial infarction (MI) is a leading cause of global cardiovascular mortality.
- S100A8/A9, an alarmin released by myeloid cells, is implicated in cardiovascular disease pathogenesis.
- The specific role of S100A8/A9 in MI etiology requires further elucidation.
Purpose of the Study:
- To review the critical roles and mechanisms of S100A8/A9 in the pathogenesis of MI.
- To discuss the cellular sources of S100A8/A9 in infarcted hearts.
- To explore the predictive value of S100A8/A9 in cardiovascular event recurrence.
Main Methods:
- Literature review focusing on S100A8/A9 in myocardial infarction.
- Analysis of S100A8/A9's role in different stages of MI and ischemia/reperfusion (I/R) injury.
- Examination of S100A8/A9's predictive capacity for cardiovascular event recurrence.
Main Results:
- S100A8/A9 contributes to pathogenesis during both early inflammation and late repair phases of MI.
- The S100A8/A9 heterodimer impacts myocardial ischemia/reperfusion (I/R) injury.
- Elevated S100A8/A9 levels predict a higher risk of recurrent cardiovascular events.
Conclusions:
- S100A8/A9 is a significant driver of MI pathogenesis through various molecular mechanisms.
- S100A8/A9 presents potential as a predictive biomarker for cardiovascular event recurrence.
- Targeting S100A8/A9 offers a promising therapeutic strategy for MI.
Abstract:
Myocardial infarction (MI), the main cause of cardiovascular-related deaths worldwide, has long been a hot topic because of its threat to public health. S100A8/A9 has recently attracted an increasing amount of interest as a crucial alarmin that regulates the pathogenesis of cardiovascular disease after its release from myeloid cells. However, the role of S100A8/A9 in the etiology of MI is not well understood. Here, we elaborate on the critical roles and potential mechanisms of S100A8/A9 driving the pathogenesis of MI. First, cellular source of S100A8/A9 in infarcted heart is discussed. Then we highlight the effect of S100A8/A9 heterodimer in the early inflammatory period and the late reparative period of MI as well as myocardial ischemia/reperfusion (I/R) injury. Moreover, the predictive value of S100A8/A9 for the risk of recurrence of cardiovascular events is elucidated. Therefore, this review focuses on the molecular mechanisms of S100A8/A9 in MI pathogenesis to provide a promising biomarker and therapeutic target for MI.
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