Sex differences in immune response and hormones like testosterone increase inflammation and reactive oxygen species production in male-dominant autoimmune viral myocarditis.
This review outlines the mechanisms underlying sex differences in myocarditis, emphasizing the role of testosterone in exacerbating inflammation via TLR4 and inflammasome pathways.
Autoimmune diseases are characterized by circulating antibodies and immune complexes directed against self-tissues that result in both systemic and organ-specific inflammation and pathology. Most autoimmune diseases occur more often in women than men. One exception is myocarditis, which is an inflammation of the myocardium that is typically caused by viral infections. Sex differences in the immune response and the role of the sex hormones estrogen and testosterone are well established based on animal models of autoimmune viral myocarditis as well as in mitochondrial function leading to reactive oxygen species production. RNA viruses like coxsackievirus B3, the primary cause of myocarditis in the US, activate the inflammasome through mitochondrial antiviral signaling protein located on the mitochondrial outer membrane. Toll-like receptor 4 and the inflammasome are the primary signaling pathways that increase inflammation during myocarditis, which is increased by testosterone. This review describes what is known about sex differences in inflammation, redox biology and mitochondrial function in the male-dominant autoimmune disease myocarditis and highlights gaps in the literature and future directions.
Florio et al. (Wed,) conducted a review in Myocarditis. Sex differences was evaluated. Sex differences in immune response and hormones like testosterone increase inflammation and reactive oxygen species production in male-dominant autoimmune viral myocarditis.
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