Akademik Veri Yönetim Sistemi
UHOD-ULUSLARARASI HEMATOLOJI-ONKOLOJI DERGISI, cilt.30, sa.2, ss.113-120, 2020 (SCI-Expanded)
For the first time on December 31, 2019, 27 cases of pneumonia of unknown etiology were detected in Wuhan City, Hubei province, China. The factor that caused this clinic was called Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). In the following days, WHO officially named the disease caused by the new coronavirus as Coronavirus Disease 2019 (COVID-19). Patients infected with SARS-CoV-2 mostly applied to health centers with symptoms of dry cough, shortness of breath and fever. some patients have developed death-causing complications such as organ failure, septic shock, pulmonary edema, severe pneumonia, and Acute Respiratory Distress Syndrome (ARDS). SARS-CoV-2 infects patients by binding human Angiotensin Converting Enzyme 2 (ACE 2), causing to severe pneumonia and high mortality. Circulating RAS and local paracrin-autocrin-intracrin tissue-based RAS participate in numerous pathobiological events. Pro-inflammatory, pro-fibrotic, and pro-thrombotic consequences associated with local RAS activation have been detected at cellular and molecular level. Regenerative progenitor cell therapy in response to RAS-modulating pharmacotherapy in context of endothelial cell damage and regeneration emerged as an auxiliary therapy to improve regeneration of the vascular endothelium. The aim of this article is to evaluate the relationship between circulating and local angiotensin systems and COVID-19.