Key result
TGF-β, CTGF, RAS, and ncRNAs drive cardiomyocyte-fibroblast crosstalk during ischemia/reperfusion injury, offering therapeutic targets.
Why the study?
Despite success in animal models, therapies protecting cardiac tissue from reperfusion-induced injury have not completely translated to human applications.
Elucidating the molecular crosstalk between cardiomyocytes and fibroblasts during ischemia/reperfusion injury may identify novel therapeutic targets to prevent adverse cardiac remodeling.
Should not yet change ischemia/reperfusion management; leaves open validation of TGF-β, CTGF, and non-coding RNA targets in trials.
Communication between cells is a foundational concept for understanding the physiology and pathology of biological systems. Paracrine/autocrine signaling, direct cell-to-cell interplay, and extracellular matrix interactions are three types of cell communication that regulate responses to different stimuli. In the heart, cardiomyocytes, fibroblasts, and endothelial cells interact to form the cardiac tissue. Under pathological conditions, such as myocardial infarction, humoral factors released by these cells may induce tissue damage or protection, depending on the type and concentration of molecules secreted. Cardiac remodeling is also mediated by the factors secreted by cardiomyocytes and fibroblasts that are involved in the extensive reciprocal interactions between these cells. Identifying the molecules and cellular signal pathways implicated in these processes will be crucial for creating effective tissue-preserving treatments during or after reperfusion. Numerous therapies to protect cardiac tissue from reperfusion-induced injury have been explored, and ample pre-clinical research has attempted to identify drugs or techniques to mitigate cardiac damage. However, despite great success in animal models, it has not been possible to completely translate these cardioprotective effects to human applications. This review provides a current summary of the principal molecules, pathways, and mechanisms underlying cardiomyocyte and cardiac fibroblast crosstalk during ischemia/reperfusion injury. We also discuss pre-clinical molecules proposed as treatments for myocardial infarction and provide a clinical perspective on these potential therapeutic agents.
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Flores-Vergara et al. (2021) conducted a review in Myocardial infarction and ischemia/reperfusion injury. Cardiomyocyte and cardiac fibroblast crosstalk during ischemia/reperfusion injury is mediated by TGF-β, CTGF, the renin-angiotensin system, and non-coding RNAs, offering potential therapeutic targets.
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