excellent review on cardioimmunology by Filip K. Swirski & Matthias Nahrendorf (Cardioimmunology: the immune system in cardiac homeostasis and disease. Nat. Rev. Immunol. 18, 733–744 (2018))1. The authors extensively discussed… Click to show full abstract
excellent review on cardioimmunology by Filip K. Swirski & Matthias Nahrendorf (Cardioimmunology: the immune system in cardiac homeostasis and disease. Nat. Rev. Immunol. 18, 733–744 (2018))1. The authors extensively discussed the role of immune cells in normal and diseased heart, specifically in myocardial infarction, myocarditis and endocarditis, heart failure and rhythm disorders1. Regarding rhythm disorders, they speculated that the immune immuno-cardiac electrophysiology. In fact, accumulating data indicate that the immune system can promote cardiac arrhythmias by means of autoantibodies and/or inflammatory cytokines that directly affect the function of specific ion channels on the surface of cardiomyocytes2–4. Several autoantibodies have been described that target cardiac Ca2+, K+ or Na+ channels and that have arrhythmogenic effects in the absence of evident histological changes in the heart; these are known as autoimmune cardiac channelopathies2,4. Indeed, it is well recognized that antiSjögren’ssyndrome-related antigen A (antiSSA) antibodies (also known as antiRo/SSA antibodies) can cross react with the pore region of both Ltype Ca2+ channels (CaV1.2 and CaV1.3) and Ttype Ca2+ channels (CaV3.1 and CaV3.2). By inhibiting the related Ca2+ currents, these antibodies promote conduction disturbances, such as sinus bradycardia and atrioventricular (AV) block5,6 (Fig. 1a). Similar clinical consequences were also shown for autoantibodies recognizing the extracellular loop of domain system could contribute to arrhythmias through two mechanisms — a crosstalk between immune cells and fibroblasts and/or myocytes, leading to insulating fibrosis, or a direct participation of leukocytes (macrophages) in the electrical regulation of conducting cells, by interacting through connexin 43 (CX43)-containing gap junctions1. However, the authors substantially disregarded a third important mechanism of arrhythmias in this new field of Cardioimmunology of arrhythmias: the role of autoimmune and inflammatory cardiac channelopathies
               
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