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10.1002/iid3.638

http://scihub22266oqcxt.onion/10.1002/iid3.638
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35759228!9186334!35759228
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suck abstract from ncbi


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pmid35759228      Immun+Inflamm+Dis 2022 ; 10 (7): e638
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  • An alternative way of SARS-COV-2 to induce cell stress and elevated DNA damage risk in cardiomyocytes without direct infection #MMPMID35759228
  • Zhou H; Ren X; Yang Y; Xu B; Li Y; Feng Y; Shisong F; Liu J
  • Immun Inflamm Dis 2022[Jul]; 10 (7): e638 PMID35759228show ga
  • BACKGROUND: The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) in 2020 has led to millions of deaths worldwide. Case reports suggested that infection of SARS-CoV-2 is potentially associated with occurrences of cardiovascular pathology. However, the mode of action and mechanisms of SARS-CoV-2 influencing cardiomyocytes still remain largely unclear. AIMS: To explore the mechanisms underlying cardiomyocytes damage induced by SARS-CoV-2 infection. MATERIALS & METHODS: the serum markers of cardiovascular injury were analyzed by ELISA. The isolated SARS-CoV-2 virus were co-cultured with human cardiomyocytes (AC16) and immunofluorescence assay was used evaluate the invasion of virus. 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. RESULTS: we found that high-sensitivity troponin T (hsTnT), an indicator of cardiovascular disease, was higher in the acute stage of COVID-19. 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 of serum treatment suggested that serum from infected subjects induced cell stress (upregulation of p53 and HSP70) and elevation of DNA damage risk (increased gammaH2Ax and H3K79me2) in AC16. DISCUSSION: our observations indicated a hard way for SARS-CoV-2 to infect cardiomyocytes directly. However, infection-induced immune storm in serum could bring stress and elevated DNA damage risks to cardiovascular system. CONCLUSION: These findings indicated the possibilities of SARS-CoV-2 inducing stress and elevating DNA damage risk to cardiomyocytes without direct infection.
  • |*COVID-19[MESH]
  • |*SARS-CoV-2[MESH]
  • |DNA Damage[MESH]
  • |Humans[MESH]


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