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Converging pathways in pulmonary fibrosis and Covid-19 - The fibrotic link to disease severity : Common molecular pathways in Covid-19 and pulmonary fibrosis

Wigén, Jenny LU ; Löfdahl, Anna LU ; Bjermer, Leif LU ; Elowsson-Rendin, Linda LU and Westergren-Thorsson, Gunilla LU orcid (2020) In Respiratory Medicine: X 2.
Abstract

As Covid-19 affects millions of people worldwide, the global health care will encounter an increasing burden of the aftermaths of the disease. Evidence shows that up to a fifth of the patients develop fibrotic tissue in the lung. The SARS outbreak in the early 2000 resulted in chronic pulmonary fibrosis in a subset (around 4%) of the patients, and correlated to reduced lung function and forced expiratory volume (FEV). The similarities between corona virus infections causing SARS and Covid-19 are striking, except that the novel coronavirus, SARS-CoV-2, has proven to have an even higher communicability. This would translate into a large number of patients seeking care for clinical signs of pulmonary fibrosis, given that the Covid-19... (More)

As Covid-19 affects millions of people worldwide, the global health care will encounter an increasing burden of the aftermaths of the disease. Evidence shows that up to a fifth of the patients develop fibrotic tissue in the lung. The SARS outbreak in the early 2000 resulted in chronic pulmonary fibrosis in a subset (around 4%) of the patients, and correlated to reduced lung function and forced expiratory volume (FEV). The similarities between corona virus infections causing SARS and Covid-19 are striking, except that the novel coronavirus, SARS-CoV-2, has proven to have an even higher communicability. This would translate into a large number of patients seeking care for clinical signs of pulmonary fibrosis, given that the Covid-19 pandemic has up till now (Sept 2020) affected around 30 million people. The SARS-CoV-2 is dependent on binding to the angiotensin converting enzyme 2 (ACE2), which is part of the renin-angiotensin system (RAS). Downregulation of ACE2 upon virus binding disturbs downstream activities of RAS resulting in increased inflammation and development of fibrosis. The poor prognosis and risk of developing pulmonary fibrosis are therefore associated with the increased expression of ACE2 in risk groups, such as obesity, heart disorders and aging, conferring plenty of binding opportunity for the virus and subsequently the internalization of ACE2, thus devoiding the enzyme from acting counter-inflammatory and antifibrotic. Identifying pathways that are associated with Covid-19 severity that result in pulmonary fibrosis may enable early diagnosis and individualized treatment for these patients to prevent or reduce irreversible fibrotic damage to the lung.

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author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Angiotensin converting enzyme 2 (ACE2), Chemokines, Chronic pulmonary fibrosis, Covid-19, Cytokines, Extracellular matrix, Matrix metalloproteases
in
Respiratory Medicine: X
volume
2
article number
100023
publisher
Elsevier
external identifiers
  • pmid:33083782
  • scopus:85092940353
ISSN
2590-1435
DOI
10.1016/j.yrmex.2020.100023
language
English
LU publication?
yes
id
b9276bef-eea0-4652-adc1-38a3c345902d
date added to LUP
2020-11-05 12:47:18
date last changed
2024-06-28 03:02:38
@article{b9276bef-eea0-4652-adc1-38a3c345902d,
  abstract     = {{<p>As Covid-19 affects millions of people worldwide, the global health care will encounter an increasing burden of the aftermaths of the disease. Evidence shows that up to a fifth of the patients develop fibrotic tissue in the lung. The SARS outbreak in the early 2000 resulted in chronic pulmonary fibrosis in a subset (around 4%) of the patients, and correlated to reduced lung function and forced expiratory volume (FEV). The similarities between corona virus infections causing SARS and Covid-19 are striking, except that the novel coronavirus, SARS-CoV-2, has proven to have an even higher communicability. This would translate into a large number of patients seeking care for clinical signs of pulmonary fibrosis, given that the Covid-19 pandemic has up till now (Sept 2020) affected around 30 million people. The SARS-CoV-2 is dependent on binding to the angiotensin converting enzyme 2 (ACE2), which is part of the renin-angiotensin system (RAS). Downregulation of ACE2 upon virus binding disturbs downstream activities of RAS resulting in increased inflammation and development of fibrosis. The poor prognosis and risk of developing pulmonary fibrosis are therefore associated with the increased expression of ACE2 in risk groups, such as obesity, heart disorders and aging, conferring plenty of binding opportunity for the virus and subsequently the internalization of ACE2, thus devoiding the enzyme from acting counter-inflammatory and antifibrotic. Identifying pathways that are associated with Covid-19 severity that result in pulmonary fibrosis may enable early diagnosis and individualized treatment for these patients to prevent or reduce irreversible fibrotic damage to the lung.</p>}},
  author       = {{Wigén, Jenny and Löfdahl, Anna and Bjermer, Leif and Elowsson-Rendin, Linda and Westergren-Thorsson, Gunilla}},
  issn         = {{2590-1435}},
  keywords     = {{Angiotensin converting enzyme 2 (ACE2); Chemokines; Chronic pulmonary fibrosis; Covid-19; Cytokines; Extracellular matrix; Matrix metalloproteases}},
  language     = {{eng}},
  publisher    = {{Elsevier}},
  series       = {{Respiratory Medicine: X}},
  title        = {{Converging pathways in pulmonary fibrosis and Covid-19 - The fibrotic link to disease severity : Common molecular pathways in Covid-19 and pulmonary fibrosis}},
  url          = {{http://dx.doi.org/10.1016/j.yrmex.2020.100023}},
  doi          = {{10.1016/j.yrmex.2020.100023}},
  volume       = {{2}},
  year         = {{2020}},
}