CaMKII Activity in the Inflammatory Response of Cardiac Diseases

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.

Improvement Effect of Lotus Leaf Flavonoids on Carbon Tetrachloride-Induced Liver Injury in Mice

“…Low concentration of TNF-α can regulate the growth, differentiation, and regeneration of hepatocytes, but high concentration TNF-α does not only induce hepatocyte apoptosis, but it is also the main factor causing hepatocyte damage [32]. NF-κB is an important transcription factor in vivo, which regulates the gene expression required for an inflammatory response, such as liver injury [33]. High NF-κB level indicates liver injury [34].…”

Preventive effect of lemon seed flavonoids on carbon tetrachloride-induced liver injury in mice

“…IkB-a binds activated NF-kB to inhibit inammation. 41 NO is a highly active oxidant, generated by activated NOS in hepatocytes. It can promote the high gene expression of iNOS aer liver injury develops to the decompensated stage.…”

Fibrosis in Arrhythmogenic Cardiomyopathy: The Phantom Thread in the Fibro-Adipose Tissue

“…An important independent fibrosis cofactor in ACM hearts is inflammation. ACM hearts are characterized by progressive CM death that is replaced by non-contractile fibrotic tissue according to a reparative mechanism against myocardial loss (Valente et al, 1998;Rusciano et al, 2019).…”