Evidence map›Paper›PMID 33083782›Full record

ReviewRespiratory medicine: X2020

Converging pathways in pulmonary fibrosis and Covid-19 - The fibrotic link to disease severity.

Jenny Wigén, Anna Löfdahl, Leif Bjermer, Linda Elowsson-Rendin, Gunilla Westergren-Thorsson

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in Respiratory medicine: X, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07380152 (Corticosteroid Treatment for Post-COVID-19 Persistent Interstitial Lung Disease), which is not on this map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
1.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT07380152 phase1completednot on this mapstarted 2021, after this paper: background citation

Corticosteroid Treatment for Post-COVID-19 Persistent Interstitial Lung Disease

TypeinterventionalSponsorUniversity of Sao PauloRan2021 to 2022Enrolled100ConditionsCOVID-19 Pulmonary ComplicationsArmsPrednisolone
3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Jenny WigénLung Biology Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Anna LöfdahlLung Biology Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Leif BjermerDepartment of Clinical Sciences, Lund, Respiratory Medicine and Allergology, Lund University, Lund, Sweden.
Linda Elowsson-RendinLung Biology Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Gunilla Westergren-ThorssonLung Biology Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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 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.

Indexed as

Angiotensin converting enzyme 2 (ACE2)ChemokinesChronic pulmonary fibrosisCovid-19CytokinesExtracellular matrixMatrix metalloproteases

Identifiers

PMID33083782
PMCPMC7546672
OpenAlexW3092466163

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.