Role of pirfenidone in TGF-β pathways and other inflammatory pathways in acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection: a theoretical perspective
Open accessAbstract
Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes pulmonary injury or multiple-organ injury by various pathological pathways. Transforming growth factor-beta (TGF-β) is a key factor that is released during SARS-CoV-2 infection. TGF-β, by internalization of the epithelial sodium channel (ENaC), suppresses the anti-oxidant system, downregulates the cystic fibrosis transmembrane conductance regulator (CFTR), and activates the plasminogen activator inhibitor 1 (PAI-1) and nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-kB). These changes cause inflammation and lung injury along with coagulopathy. Moreover, reactive oxygen species play a significant role in lung injury, which levels up during SARS-CoV-2 infection.Drug suggestion Pirfenidone is an anti-fibrotic drug with an anti-oxidant activity that can prevent lung injury during SARS-CoV-2 infection by blocking the maturation process of transforming growth factor-beta (TGF-β) and enhancing the protective role of peroxisome proliferator-activated receptors (PPARs). Pirfenidone is a safe drug for patients with hypertension or diabetes and its side effect tolerated well.Conclusion The drug as a theoretical perspective may be an effective and safe choice for suppressing the inflammatory response during COVID-19. The recommendation would be a combination of pirfenidone and N-acetylcysteine to achieve maximum benefit during SARS-CoV-2 treatment.
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PFD reduces fibroblast proliferation and inhibits the TGF-β pathway.
“PFD reduces fibroblast proliferation and inhibits transforming growth factor–β (TGF-β) pathway (28).”
From Modeling mechanical activation of macrophages during pulmonary fibrogenesis for targeted anti-fibrosis therapy (2024) · cites this paper as [28]
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References 146 · Cited by 50
Research works printed but not linked: 2
- [8]Weber G Advances in enzyme regulation 2003 Amsterdam Elsevier
- [56]Matthay MA Acute respiratory distress syndrome 2003 Boca Raton CRC Press
- Authors
- Hamidi, S. H., Kadamboor Veethil, S., & Hamidi, S. H.
- Affiliations
- Rajiv Gandhi University of Health Sciences (IN)
- Corresponding author
- Hamidi, Seyed Hootan
- ORCID
- Hamidi, Seyed Hootan
- Venue
- Pharmacological Reports
- Published
- 2021-04-21
- Volume
- 73
- Issue
- 3
- Pages
- 712-727
- ISSN
- 1734-1140 (ISSN-L)
- 2299-5684
- PMC
- PMC8057922
- OpenAlex
- W3153994448
- Cited by
- 50
- References
- 146
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 13 · 2023: 12 · 2022: 12 · 2021: 2
- FWCI
- 1.14
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Pharmacological Reports (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Keywords
- pirfenidone, SARS-CoV-2, COVID-19 pandemic, TGF-beta signaling, lung injury, inflammation, oxidative stress, reactive oxygen species, NF-κB, plasminogen activator inhibitor-1, CFTR, epithelial sodium channel, peroxisome proliferator-activated receptors, N-acetylcysteine, antifibrotic therapy, coagulopathy
- MeSH terms
- COVID-19, SARS-CoV-2, COVID-19 Drug Treatment, Anti-Inflammatory Agents, Non-Steroidal, Humans, Inflammation, Pyridones, Signal Transduction, Transforming Growth Factor beta, Lung Injury
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