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Multi-organ failure in COVID-19 patients: A possible mechanistic approach
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  • Umashanker Navik,
  • Jasvinder Bhatti,
  • Vaibhav Sheth,
  • Snehal Jawalekar,
  • Gurjit Bhatti,
  • Sourav Kalra
Umashanker Navik
Central University of Punjab
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Jasvinder Bhatti
Central University of Punjab
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Vaibhav Sheth
National Institute of Pharmaceutical Education and Research
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Snehal Jawalekar
National Institute of Pharmaceutical Education and Research
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Gurjit Bhatti
Chandigarh University
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Sourav Kalra
National Institute of Pharmaceutical Education and Research
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Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel single-stranded RNA virus and induces cytokines storm that play a crucial role in the pathogenetic mechanisms of acute respiratory distress syndrome and the subsequent multi-organ failure. SARS-CoV-2 enters the host cell through angiotensin-converting enzyme 2 (ACE 2) receptor and patients with forgoing chronic diseases are most vulnerable to SARS-CoV-2 infection and increase the mortality. ACE 2 is part of the renin-aldosterone angiotensin system (RAAS) which is highly expressed in the intestine, pancreas, kidney, heart, lungs, liver, maternal-fetal interface and fetal tissues. RAAS system is dysregulated in patients underlying hypertension, cardiovascular diseases, diabetes, renal disorder and preeclampsia. Drugs acting on the RAAS system, thiazolidinediones and smoking, preeclampsia, chronic liver diseases up-regulates the ACE 2 expression that may act as an entry point for SARS-CoV-2 and leading to multi-organ failure with a massive release of cytokines. Hence, this review shed a light on a path of increased mortality rate among COVID-19 patients and the possible mechanism of multi-organ failure.