4.7 Article

The probable role and therapeutic potential of the PI3K/AKT signaling pathway in SARS-CoV-2 induced coagulopathy

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BMC
DOI: 10.1186/s11658-022-00308-w

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SARS-CoV-2; Coagulation; COVID-19; PI3K; AKT

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COVID-19, caused by SARS-CoV-2, has a high mortality rate primarily due to ARDS, cytokine storm, and coagulation complications. Although changes in coagulation factors have been observed in COVID-19 patients, the specific molecular mechanism has not yet been explored. However, the over-activity of the PI3K/AKT signaling pathway in SARS-CoV-2 infection suggests its potential role as a therapeutic target for preventing coagulation complications in COVID-19 patients.
Coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), is associated with a high mortality rate. The majority of deaths in this disease are caused by ARDS (acute respiratory distress syndrome) followed by cytokine storm and coagulation complications. Although alterations in the level of the number of coagulation factors have been detected in samples from COVID-19 patients, the direct molecular mechanism which has been involved in this pathologic process has not been explored yet. The PI3K/AKT signaling pathway is an intracellular pathway which plays a central role in cell survival. Also, in recent years the association between this pathway and coagulopathies has been well clarified. Therefore, based on the evidence on over-activity of the PI3K/AKT signaling pathway in SARS-CoV-2 infection, in the current review, the probable role of this cellular pathway as a therapeutic target for the prevention of coagulation complications in patients with COVID-19 is discussed.

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