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Review
. 2023 Jun;1(2):77-83.
doi: 10.1016/j.pccm.2022.12.002. Epub 2023 Jan 23.

Pulmonary fibrosis: A short- or long-term sequelae of severe COVID-19?

Zhen Zheng  1 , Fei Peng  1   2 , Yong Zhou  1
Affiliations
Review

Pulmonary fibrosis: A short- or long-term sequelae of severe COVID-19?

Zhen Zheng et al. Chin Med J Pulm Crit Care Med. 2023 Jun.

Abstract

The pandemic of coronavirus disease 2019 (COVID‑19), caused by a novel severe acute respiratory syndrome (SARS) coronavirus 2 (SARS-CoV-2), has caused an enormous impact on the global healthcare. SARS-CoV-2 infection primarily targets the respiratory system. Although most individuals testing positive for SARS-CoV-2 present mild or no upper respiratory tract symptoms, patients with severe COVID-19 can rapidly progress to acute respiratory distress syndrome (ARDS). ARDS-related pulmonary fibrosis is a recognized sequelae of COVID-19. Whether post-COVID-19 lung fibrosis is resolvable, persistent, or even becomes progressive as seen in human idiopathic pulmonary fibrosis (IPF) is currently not known and remains a matter of debate. With the emergence of effective vaccines and treatments against COVID-19, it is now important to build our understanding of the long-term sequela of SARS-CoV-2 infection, to identify COVID-19 survivors who are at risk of developing chronic pulmonary fibrosis, and to develop effective anti-fibrotic therapies. The current review aims to summarize the pathogenesis of COVID-19 in the respiratory system and highlights ARDS-related lung fibrosis in severe COVID-19 and the potential mechanisms. It envisions the long-term fibrotic lung complication in COVID-19 survivors, in particular in the aged population. The early identification of patients at risk of developing chronic lung fibrosis and the development of anti-fibrotic therapies are discussed.

Keywords: Coronavirus disease 2019 (COVID‑19); Lung fibrosis; Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

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Conflict of interest statement

None.

Figures

Fig 1
Fig. 1
Potential mechanisms underlying pulmonary fibrosis associated with COVID-19. Diagram was created via Biorender.com. ACE2: Angiotensin-converting enzyme 2; Ang II: Angiotensin II; Ang-(1–7): Angiotensin 1–7; CCL2: Monocyte chemoattractant protein-1; COVID-19: Coronavirus disease 2019; CTGF: Connective tissue growth factor; Gal-3: Galectin-3; IL: Interleukin; MV: Mechanical ventilation; RGD: Arginine (Arg)-glycine (Gly)-aspartic acid (Asp); SARS-CoV-2: Severe acute respiratory syndrome (SARS) coronavirus 2; TGF-β1: Transforming growth factor -β1; TNF: Tumor necrosis factor.
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