PMC:7340597 / 23235-24407 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7340597","sourcedb":"PMC","sourceid":"7340597","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7340597","text":"Although the exact pathogenesis of OP remains unknown, it is thought that OP is a consequence of alveolar epithelial injury. This initial epithelial injury is followed by leakage of plasma proteins, leading to a cascade of host responses with hyperinflammation [27,28]. Subsequent fibroblast recruitment and connective tissue and fibroblast organisation is seen within the alveolar space. Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) play a central role in organizing pneumonia and are highly expressed in intraluminal fibromyxoid lesion in organizing pneumonia [29]. Interestingly, binding to ACE2 receptor is recognized as a critical initial step for SARS-CoV-2 to entry alveolar type II cells, resulting in loss of ACE2 at the membrane. ACE 2 is a negative regulator of the renin-angiotensin system (RAS) and this depletion of ACE2 upregulates the RAS [30]. An activated RAS can induce Fibroblastic Growth Factor. ACE2 also plays a role in regulating the effect of VEGF [31]. Therefore, depletion of ACE2 due to the high affinity of SARS-CO-V2 to ACE2 might play a role in the pathogenesis of COVID19 related organizing 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