Two important controversial risk factors in SARS-CoV-2 infection: Obesity and smoking

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ENGİN A. B., ENGİN E. D., Engin A.

ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, cilt.78, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 78
  • Basım Tarihi: 2020
  • Doi Numarası: 10.1016/j.etap.2020.103411
  • Dergi Adı: ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Agricultural & Environmental Science Database, BIOSIS, CAB Abstracts, EMBASE, Environment Index, Greenfile, MEDLINE, Pollution Abstracts, Veterinary Science Database
  • Anahtar Kelimeler: COVID-19, Angiotensin II, Smoking, Air pollution, Obesity, Angiotensin-converting-enzyme inhibitors, RENIN-ANGIOTENSIN SYSTEM, CONVERTING ENZYME 2, ALDOSTERONE SYSTEM, SARS CORONAVIRUS, RECEPTOR-BINDING, ACE2, OUTCOMES, INSULIN, TMPRSS2, STRESS
  • Gazi Üniversitesi Adresli: Evet

Özet

The effects of obesity and smoking in the coronavirus disease 2019 (COVID-19) pandemic remain controversial. Angiotensin converting enzyme 2 (ACE2), a component of the renin-angiotensin system (RAS), is the human cell receptor of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of COVID-19. ACE2 expression increases on lung alveolar epithelial cells and adipose tissue due to obesity, smoking and air pollution. A significant relationship exists between air pollution and SARS-CoV-2 infection, as more severe COVID-19 symptoms occur in smokers; comorbid conditions due to obesity or excess ectopic fat accumulation as underlying risk factors for severe COVID-19 strongly encourage the virus/ACE2 receptor-ligand interaction concept. Indeed, obesity, air pollution and smoking associated risk factors share underlying pathophysiologies that are related to the Renin-Angiotensin-System in SARS-CoV-2 infection. The aim of this review is to emphasize the mechanism of receptor-ligand interaction and its impact on the enhanced risk of death due to SARS-CoV-2 infection.