Key result
CaMKII acts as an inflammatory mediator in heart and kidney interactions, though its specific role in cardiorenal syndrome remains poorly understood and requires further investigation.
Why the study?
Cardiorenal syndrome is an increasingly pressing issue, yet very little is known about the role of CaMKII as an inflammatory mediator in heart and kidney interaction.
This review highlights the need for further investigation into the role of CaMKII as an inflammatory mediator in cardiorenal syndrome.
CaMKII may link calcium signaling to inflammation in CRS; leaves open whether targeting it improves cardiorenal outcomes.
Calcium/calmodulin-dependent protein kinases (CaMKs) are key regulators of calcium signaling in health and disease. CaMKII is the most abundant isoform in the heart; although classically described as a regulator of excitation-contraction coupling, recent studies show that it can also mediate inflammation in cardiovascular diseases (CVDs). Among CVDs, cardiorenal syndrome (CRS) represents a pressing issue to be addressed, considering the growing incidence of kidney diseases worldwide. In this review, we aimed to discuss the role of CaMK as an inflammatory mediator in heart and kidney interaction by conducting an extensive literature review using the database PubMed. Here, we summarize the role and regulating mechanisms of CaMKII present in several quality studies, providing a better understanding for future investigations of CamKII in CVDs. Surprisingly, despite the obvious importance of CaMKII in the heart, very little is known about CaMKII in CRS. In conclusion, more studies are necessary to further understand the role of CaMKII in CRS.
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Junho et al. (2020) conducted a review in Cardiorenal Syndrome. Calcium/calmodulin-dependent protein kinase II (CaMKII) was evaluated. CaMKII acts as an inflammatory mediator in heart and kidney interactions, though its specific role in cardiorenal syndrome remains poorly understood and requires further investigation.
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