Why the study?
Common heart diseases lack effective therapy due to complex pathogenesis, and the exact roles and pathophysiological pathways of interleukins across primary cardiac cell types remain largely unexplored.
This review highlights the cell-specific pathophysiological roles of various interleukins in heart diseases, suggesting potential targets for more precise therapies.
Cell-specific targeting may offer a path forward in MI/HF; leaves open clinical translation pending prospective trials.
Myocardial infarction (MI), heart failure, cardiomyopathy, myocarditis, and myocardial ischemia-reperfusion injury (I/R) are the most common heart diseases, yet there is currently no effective therapy due to their complex pathogenesis. Cardiomyocytes (CMs), fibroblasts (FBs), endothelial cells (ECs), and immune cells are the primary cell types involved in heart disorders, and, thus, targeting a specific cell type for the treatment of heart disease may be more effective. The same interleukin may have various effects on different kinds of cell types in heart disease, yet the exact role of interleukins and their pathophysiological pathways on primary cell types remain largely unexplored. This review will focus on the pathophysiological effects of various interleukins including the IL-1 family (IL-1, IL-18, IL-33, IL-37), IL-2, IL-4, the IL-6 family (IL-6 and IL-11), IL-8, IL-10, IL-17 on primary cell types in common heart disease, which may contribute to the more precise and effective treatment of heart disease.
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Liu et al. (2023) studied this question.
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