Comprehensive overview of COVID-19-related respiratory failure: focus on cellular interactions

Fahimeh Zamani Rarani, Mohammad Zamani Rarani, Michael R. Hamblin, Bahman Rashidi, Seyed Mohammad Reza Hashemian, Hamed Mirzaei

Research output: Contribution to journalReview articlepeer-review

5 Citations (Scopus)


The pandemic outbreak of coronavirus disease 2019 (COVID-19) has created health challenges in all parts of the world. Understanding the entry mechanism of this virus into host cells is essential for effective treatment of COVID-19 disease. This virus can bind to various cell surface molecules or receptors, such as angiotensin-converting enzyme 2 (ACE2), to gain cell entry. Respiratory failure and pulmonary edema are the most important causes of mortality from COVID-19 infections. Cytokines, especially proinflammatory cytokines, are the main mediators of these complications. For normal respiratory function, a healthy air–blood barrier and sufficient blood flow to the lungs are required. In this review, we first discuss airway epithelial cells, airway stem cells, and the expression of COVID-19 receptors in the airway epithelium. Then, we discuss the suggested molecular mechanisms of endothelial dysfunction and blood vessel damage in COVID-19. Coagulopathy can be caused by platelet activation leading to clots, which restrict blood flow to the lungs and lead to respiratory failure. Finally, we present an overview of the effects of immune and non-immune cells and cytokines in COVID-19-related respiratory failure.

Original languageEnglish
Article number63
JournalCellular and Molecular Biology Letters
Issue number1
Publication statusPublished - Dec 2022


  • Airway epithelial cells
  • COVID-19
  • Cytokines
  • Endothelial cells
  • Platelets
  • Pulmonary edema
  • SARS-CoV-2

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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