Evidence map›Paper›PMID 36044102›Full record

ReviewInflammopharmacology2022

Pirfenidone and post-Covid-19 pulmonary fibrosis: invoked again for realistic goals.

Hayder M Al-Kuraishy, Gaber El-Saber Batiha, Hani Faidah, Ali I Al-Gareeb, Hebatallah M Saad, Jesus Simal-Gandara

Open access · greenAbstract readReview
In one paragraph

Review in Inflammopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 1% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 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

6 authors at 4 institutions in 3 countries.

Hayder M Al-KuraishyDepartment of Clinical Pharmacology and Medicine, College of Medicine, ALmustansiriyia University, M.B.Ch.B, FRCP, Baghdad, Iraq.
Gaber El-Saber BatihaDepartment of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, 22511, AlBeheira, Egypt. gaberbatiha@gmail.com.
Hani FaidahMicrobiolgy Department Faculty of Medicine, Umm Al Qura University, Mecca, Saudi Arabia.
Ali I Al-GareebDepartment of Clinical Pharmacology and Medicine, College of Medicine, ALmustansiriyia University, M.B.Ch.B, FRCP, Baghdad, Iraq.
Hebatallah M SaadDepartment of Pathology, Faculty of Veterinary Medicine, Matrouh University, Matrouh, 51744, Matrouh, Egypt. heba.magdy@mau.edu.eg.ORCID http://orcid.org/0000-0001-9555-7300
Jesus Simal-GandaraNutrition and Bromatology Group, Department of Analytical Chemistry and Food Science, Faculty of Science, Universidade de Vigo, E-32004, Ourense, Spain. jsimal@uvigo.es.
Damanhour University · EGEgypt Nanotechnology Center · EGUmm al-Qura University · SAUniversidade de Vigo · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pirfenidone (PFN) is an anti-fibrotic drug with significant anti-inflammatory property used for treatment of fibrotic conditions such as idiopathic pulmonary fibrosis (IPF). In the coronavirus disease 2019 (Covid-19) era, severe acute respiratory syndrome 2 (SARS-CoV-2) could initially lead to acute lung injury (ALI) and in severe cases may cause acute respiratory distress syndrome (ARDS) which is usually resolved with normal lung function. However, some cases of ALI and ARDS are progressed to the more severe critical stage of pulmonary fibrosis commonly named post-Covid-19 pulmonary fibrosis which needs an urgent address and proper management. Therefore, the objective of the present study was to highlight the potential role of PFN in the management of post-Covid-19 pulmonary fibrosis. The precise mechanism of post-Covid-19 pulmonary fibrosis is related to the activation of transforming growth factor beta (TGF-β1), which activates the release of extracellular proteins, fibroblast proliferation, fibroblast migration and myofibroblast conversion. PFN inhibits accumulation and recruitment of inflammatory cells, fibroblast proliferation, deposition of extracellular matrix in response to TGFβ1 and other pro-inflammatory cytokines. In addition, PFN suppresses furin (TGFβ1 convertase activator) a protein effector involved in the entry of SARS-CoV-2 and activation of TGFβ1, and thus PFN reduces the pathogenesis of SARS-CoV-2. Besides, PFN modulates signaling pathways such as Wingless/Int (Wnt/β-catenin), Yes-Associated Protein (YAP)/Transcription Co-Activator PDZ Binding Motif (TAZ) and Hippo Signaling Pathways that are involved in the pathogenesis of post-Covid-19 pulmonary fibrosis. In conclusion, the anti-inflammatory and anti-fibrotic properties of PFN may attenuate post-Covid-19 pulmonary fibrosis.

Indexed as

Acute Lung InjuryCOVID-19 Drug TreatmentPulmonary FibrosisRespiratory Distress SyndromeFibrosisGoalsHumansPyridonesSARS-CoV-2pirfenidonePyridonesAnti-FibroticAnti-InflammatoryCovid-19PirfenidonePulmonary Fibrosis

Identifiers

PMID36044102
PMCPMC9430017
OpenAlexW4293802328

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.