Association of Complement and MAPK Activation With SARS-CoV-2–Associated Myocardial Inflammation

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Abstract
Inflammatory cardiomyopathy is a common condition characterized by cardiac immune cell infiltration. It can be complicated by heart failure and is associated with adverse outcomes.1 Although the condition is predominantly caused by viral infections, a broad variety of factors, including systemic immune disorders and the toxic effects of medications, can produce tissue inflammation and fibrosis leading to impaired cardiac function.2 Inflammatory cardiomyopathy has recently been observed in autopsies of patients with SARS-CoV-2 infection.3 Furthermore, high cardiac troponin levels indicative of myocardial injury have been frequently reported among hospitalized patients with SARS-CoV-2 infection,4 and myocardial inflammation may persist in individuals who recovered from this disease.5 Thus, SARS-CoV-2 infection may be associated with inflammatory cardiomyopathy; however, the molecular signatures underlying this condition have remained elusive.

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