Discharge may not be the end of treatment: Pay attention to pulmonary fibrosis caused by severe COVID-19

J Med Virol. 2021 Mar;93(3):1378-1386. doi: 10.1002/jmv.26634. Epub 2020 Nov 1.

Abstract

Since December 2019, coronavirus disease (COVID-19) has rapidly swept the world. So far, more than 30 million people have been infected and nearly one million have died. Although the world is still in the stage of COVID-19 pandemic, the treatment of new cases and critically ill patients is the focus of the current work. However, COVID-19 patients lead to pulmonary fibrosis, such a serious threat to the prognosis of complications were also worthy of our attention. First of all, we proposed the possible mechanism of pulmonary fibrosis caused by SARS-CoV-2, based on the published data of COVID-19 ((i) Direct evidence: pulmonary fibrosis was found in autopsy and pulmonary puncture pathology. (ii) Indirect evidence: increased levels of fibrosis-related cytokines[transforming growth factor [TGF]- β, tumor necrosis factor [TNF]- α, interleukin [IL]-6, etc] in peripheral blood of severe patients.) What is more, we summarized the role of three fibrosis-related signaling pathways (TGF- β signal pathway, WNT signal pathway and YAP/TAZ signal pathway) in pulmonary fibrosis. Finally, we suggested the therapeutic value of two drugs (pirfenidone and nintedanib) for idiopathic pulmonary fibrosis in COVID-19-induced pulmonary fibrosis.

Keywords: COVID-19; fibrosis related signal pathway; pulmonary fibrosis; treatment.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • COVID-19 / complications*
  • COVID-19 / metabolism
  • COVID-19 / pathology
  • Humans
  • Indoles / therapeutic use*
  • Lung / pathology
  • Patient Discharge
  • Pulmonary Fibrosis / drug therapy*
  • Pulmonary Fibrosis / etiology*
  • Pulmonary Fibrosis / metabolism
  • Pulmonary Fibrosis / pathology
  • Pyridones / therapeutic use*
  • Severity of Illness Index
  • Signal Transduction

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Indoles
  • Pyridones
  • pirfenidone
  • nintedanib