Unraveling the Mechanisms of S100A8/A9 in Myocardial Injury and Dysfunction
Abstract
:1. Introduction
2. Origin and Functions of S100A8/A9
3. The Role of S100A8/A9 in Cardiac Injury
3.1. Regulating the Progression of Inflammation
3.1.1. Acting as a Mediator of Inflammation
3.1.2. Possessing Anti-Inflammatory Properties
3.2. Causing Mitochondrial Dysfunction
3.3. Modulating Myocardial Fibrosis Progression
3.4. Regulating Autophagy and Apoptosis
4. S100A8/A9: A Biomarker for Cardiovascular Disease
5. Discussion
6. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Major Methods | Diseases | Biomarker Effects |
---|---|---|
Laboratory | ||
Immunohistochemistry | Acute coronary syndrome (ACS) | Associated with thrombus formation [69] |
Proteomic comparison Immunohistochemistry and qPCR | Coronary artery disease (CAD) | Improved risk prediction and diagnostics [70] Useful for risk stratification in advanced cases [71] |
Neutrophil proteome and echocardiography assessments | Myocardial infarction (MI) | A functional biomarker for infarct wall thinning [72] |
Functional and transcriptomic analyses of extracellular vesicles | Peripheral arterial disease (PAD) | Associated with increased amputation risk [73] |
Specific ELISAs | Lymphocytic myocarditis (MC) | Served as an additional diagnostic tool [74] |
Commercial ELISA | Takayasu arteritis (TA) | Prognostic implications [75] |
Quantitative proteomic analysis | Thromboangiitis obliterans (TAO) | Implicated in TAO development [76] |
Clinical | ||
Short-term prognostic value of S100A8/A0 serum levels was determined Plasma MRP-8/14 and urinary 11-dehydro-TXB2 levels in patients were evaluated | Acute coronary syndrome (ACS) | Correlated with the number of coronary lesion branches [77] A target to test different antiplatelet strategies in ACS [78] |
The association between S100A8/A9 release and anti-inflammatory glucocorticoid secretion parameters was studied | Coronary artery disease (CAD) | May be associated with dysregulated cortisol secretion [79] |
The correlation between plasma BPI levels and circulating inflammatory biomarker levels was explored Serum S100A8/A9 levels were serially measured Various markers of NETosis were measured Serum concentrations of S100A8/A9 and high-sensitivity C-reactive protein (hs-CRP) were assessed and compared | Myocardial infarction (MI) | Positively correlated with plasma BPI levels [80] Implicated in the pathophysiology of AMI [3,81] Reducing S100A8/A9 release could reduce post-MI inflammation [82] Related to the development of very late stent thrombosis (VLST) [83] |
Blood samples were collected for biomarker calculation | Peripheral arterial disease (PAD) | Both higher mean levels and a favorable variation profile [84] |
Differences in the myocardial proteome were evaluated | Dilated cardiomyopathy (DCM) | Developed as a classifier [85] |
The distribution of platelet S100A8/A9 protein, etc., was detected | Cardiovascular complications of other diseases | Strongly and positively correlated with myoglobin, etc. [86,87,88,89,90,91,92,93,94] |
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Xu, Y.; Wang, Y.; Ning, K.; Bao, Y. Unraveling the Mechanisms of S100A8/A9 in Myocardial Injury and Dysfunction. Curr. Issues Mol. Biol. 2024, 46, 9707-9720. https://doi.org/10.3390/cimb46090577
Xu Y, Wang Y, Ning K, Bao Y. Unraveling the Mechanisms of S100A8/A9 in Myocardial Injury and Dysfunction. Current Issues in Molecular Biology. 2024; 46(9):9707-9720. https://doi.org/10.3390/cimb46090577
Chicago/Turabian StyleXu, Yuanbo, Yixuan Wang, Ke Ning, and Yimin Bao. 2024. "Unraveling the Mechanisms of S100A8/A9 in Myocardial Injury and Dysfunction" Current Issues in Molecular Biology 46, no. 9: 9707-9720. https://doi.org/10.3390/cimb46090577