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STRA6: The key to inflammatory pathways in COVID-19

Author(s): Aziz Rodan Sarohan

The COVID-19 pandemic, caused by SARS-CoV-2, has infected more than 260 million people worldwide, causing more than 5.2 million deaths. Unlike other viral infections, COVID-19 is characterized by widespread and severe systemic effects, immune dysregulation, pneumonia, ARDS, and multiple organ damage. It also causes serious inflammatory, autoimmune, endocrine, and neuropsychiatric diseases also called post-COVID syndromes. This broad spectrum of disease seen in COVID-19 cannot be explained by the previously described mechanism of viral tropism based on a single receptor mediated by ACE2 and TMPRSS2 receptors. The pathogenesis of COVID-19 can only be explained by the influence of many receptors and signaling pathways. At a crossroads in retinol metabolism and multiple inflammation-related cellular signaling pathways, STRA6 plays a key role in the pathogenesis of COVID-19. Systemic organ involvement, neuroendocrine involvement, and immunological involvement in COVID-19 can be explained very clearly through STRA6 signaling. Retinoid metabolism and STRA6 activity interact. It has been previously shown that retinol levels are reduced in COVID-19. Due to retinol depletion in COVID-19, the functions of STRA6 are also impaired. This leads to the disruption of multiple cellular signaling pathways associated with inflammation. STRA6 has a key role in the regulation of inflammatory pathways and retinoid signaling in the pathogenesis of COVID-19 and is at the center of the inflammatory process in COVID-19 due to the multiple cellular signaling pathways it directs. Targeting STRA6 and its associated signaling pathways may yield results in the prevention and treatment of many inflammatory diseases as well as COVID-19.

Journal Statistics

Impact Factor: * 5.814

CiteScore: 2.9

Acceptance Rate: 11.01%

Time to first decision: 10.4 days

Time from article received to acceptance: 2-3 weeks

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