Some theory indicates that a high inflammatory burden could be a consequence of SARS-CoV-2 infection, which potentially induces vascular inflammation, myocarditis, and cardiac arrhythmias. 7 Although many observations suggested the potential of SARS-CoV-2 inducing cardiomyocytes injury, the mode of action and mechanisms still remain largely unknown. 6 There was another retrospective study that suggested an increased risk of cardiovascular diseases, such as chronic heart failure, congenital heart disease, and chronic obstructive pulmonary disease in children infected with SARS-CoV-2. 5 A cardiovascular magnetic resonance imaging analysis was conducted on recently recovered subjects undergone SARS-CoV-2 infection and ongoing myocardial inflammation with detectable (above 3 pg/ml) high-sensitivity troponin T (hsTnT), the findings indicated the need for investigation of the long-term cardiovascular consequences after SARS-CoV-2. A cohort study analyzed 39 consecutive autopsy cases, between which 16 were found SARS-CoV-2-positive within the myocardium. 4 However, important questions remain unclear regarding the effect of SARS-CoV-2 on the cardiac system. 3 There are data pointing out an elevation of cardiovascular disease morbidity and mortality in subjects after infection of SARS-CoV-2 (approximately 12% of SARS-CoV-2 patients undergoing acute cardiac injury). 2 SARS-CoV-2 preferentially infects the low respiratory tract but is also a virus with multiorgan tropism. 1 SARS-CoV-2 is highly transmissible with a broad tissue injury including an incidence of arrhythmia. Infection of SARS-COV-2 has now spread worldwide and has become a global pandemic affecting millions of people. Severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) outbreak was first reported in December 2019, Wuhan, China. The virus caused the highly infectious disease referred to as SARS-COV-2. Conclusion: These findings indicated the possibilities of SARS-CoV-2 inducing stress and elevating DNA damage risk to cardiomyocytes without direct infection. However, infection-induced immune storm in serum could bring stress and elevated DNA damage risks to cardiovascular system. Discussion: our observations indicated a hard way for SARS-CoV-2 to infect cardiomyocytes directly. Results of serum treatment suggested that serum from infected subjects induced cell stress (upregulation of p53 and HSP70) and elevation of DNA damage risk (increased γH2Ax and H3K79me2) in AC16. Additionally, in vitro coculture of SARS-CoV-2 and AC16 cells showed almost no infectious ability of SARS-CoV-2 to directly infect AC16 cells. Results: we found that high-sensitivity troponin T (hsTnT), an indicator of cardiovascular disease, was higher in the acute stage of COVID-19. Moreover, serum obtained from acute stage of SARS-CoV-2 infected patients and healthy controls were used to incubate with AC16 cells, then indicators associated with cell stress and DNA damage were analyzed by Western-blot. The isolated SARS-CoV-2 virus were co-cultured with human cardiomyocytes (AC16) and immunofluorescence assay was used evaluate the invasion of virus. Materials & Methods: the serum markers of cardiovascular injury were analyzed by ELISA. Aims: To explore the mechanisms underlying cardiomyocytes damage induced by SARS-CoV-2 infection. However, the mode of action and mechanisms of SARS-CoV-2 influencing cardiomyocytes still remain largely unclear. Case reports suggested that infection of SARS-CoV-2 is potentially associated with occurrences of cardiovascular pathology. Background: The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) in 2020 has led to millions of deaths worldwide.
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