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Abstract
Inflammation is a physiological process by which the body responds to external insults and stress conditions, and it is characterized by the production of pro-inflammatory mediators such as cytokines. The acute inflammatory response is solved by removing the threat. Conversely, a chronic inflammatory state is established due to a prolonged inflammatory response and may lead to tissue damage. Based on the evidence of a reciprocal regulation between inflammation process and calcium unbalance, here we described the involvement of a calcium sensor in cardiac diseases with inflammatory drift. Indeed, the Ca2+/calmodulin-dependent protein kinase II (CaMKII) is activated in several diseases with an inflammatory component, such as myocardial infarction, ischemia/reperfusion injury, pressure overload/hypertrophy, and arrhythmic syndromes, in which it actively regulates pro-inflammatory signaling, among which includes nuclear factor kappa-B (NF-κB), thus contributing to pathological cardiac remodeling. Thus, CaMKII may represent a key target to modulate the severity of the inflammatory-driven degeneration.
Highlights
Inflammation is a natural and necessary immune reaction that occurs when organisms experience infections, stress, or tissue damage to fight the insulting agent
Inflammation comprises a wide range of processes that affect many aspects of normal physiology and pathology
The identification of possible modulators of the inflammatory response could be beneficial for chronic inflammatory diseases and for the diseases in which the inflammatory component represents a limit to the resolution of the pathology, such as, in the cardiac scenario, myocardial infarction, pressure overload, I/R injury, and arrhythmic diseases
Summary
Inflammation is a natural and necessary immune reaction that occurs when organisms experience infections, stress, or tissue damage to fight the insulting agent. The cells composing the heart, such as cardiomyocytes, fibroblasts, vascular cells, and progenitor cells, are able to secrete several cardiokines following different environmental stimuli, realizing a specialized network that is critical for heart homeostasis These proteins, including cytokines, such as TNF-α and TGF-β or different interleukins, are able to control the balance between normal cardiac function and pathological myocardial remodeling based on their ability to influence cardiomyocyte apoptosis, fibroblast activation, and vascular cell proliferation. The activation process requires the binding of the Ca2+/CaM complex, which displaces the intrasterical auto-inhibition and exposes the kinase substrate and ATP binding sites of the catalytic domain [36] At this point, the activated monomer is able to sequentially phosphorylate at Thr286/287 (depending on CaMKII isoforms), the regulatory domains of adjacent CaMKII monomers. CaMKII specific inhibitors increase proliferation of cardiomyocytes derived from induced pluripotent stem cells [57]
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