ReviewImmunopharmacology and immunotoxicology2021
Tranilast: a potential anti-Inflammatory and NLRP3 inflammasome inhibitor drug for COVID-19.
Review in Immunopharmacology and immunotoxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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.
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.
Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Tranilast as an Adjunctive Therapy in Hospitalized Patients with Severe COVID- 19: A Randomized Controlled Trial.Archives of medical research · 2022Trial
- Pyroptosis in chronic obstructive pulmonary disease: Beyond the canonical NLRP3/Caspase-1/GSDMD pathway.Immunologic research · 2026Review
- Exploring the Antifungal, Antibiofilm, and Wound Healing In Vitro Properties ofAntibiotics (Basel, Switzerland) · 2026Article
- The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities.MedComm · 2026Review
- Characterization of TRPV2-associated pathology in Parkinson's disease and therapeutic modulation using Tranilast.Frontiers in cellular neuroscience · 2026Article
- Targeting PANoptosis: a promising therapeutic strategy for ALI/ARDS.Apoptosis : an international journal on programmed cell death · 2025Review
- Cannabidiol inhibits TGF-β1-induced epithelial-mesenchymal transition in human conjunctival epithelial cells by interrupting TGF-β/Smad signaling.Scientific reports · 2025Article
- New Insights on the Potential Role of Pyroptosis in Parkinson's Neuropathology and Therapeutic Targeting of NLRP3 Inflammasome with Recent Advances in Nanoparticle-Based miRNA Therapeutics.Molecular neurobiology · 2025Review
- Anti-Inflammatory Potential of Essential Oil from the Heart-Wood of the Folk Medicinal TreeInternational journal of molecular sciences · 2025Article
- Computational drug discovery of phytochemical alkaloids targeting the NACHT/PYD domain in the NLRP3 inflammasome.Scientific reports · 2025Article
- Advances in acute respiratory distress syndrome: focusing on heterogeneity, pathophysiology, and therapeutic strategies.Signal transduction and targeted therapy · 2025Review
- Mechanisms and Recent Advances of Small-Molecule Therapeutics in Rosacea Treatment.Clinical, cosmetic and investigational dermatology · 2025Review
- Pharmacotherapy for Keloids and Hypertrophic Scars.International journal of molecular sciences · 2024Review
- NLRP3 Inflammasome in Autoinflammatory Diseases and Periodontitis Advance in the Management.Journal of pharmacy & bioallied sciences · 2024Review
- Review
- New Insights on NLRP3 Inflammasome: Mechanisms of Activation, Inhibition, and Epigenetic Regulation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Review
- Therapeutic Approach in Pigmented Purpuric Dermatoses-A Scoping Review.International journal of molecular sciences · 2024Article
- Inhibitors of the NLRP3 inflammasome pathway as promising therapeutic candidates for inflammatory diseases (Review).International journal of molecular medicine · 2023Review
- Race between virus and inflammasomes: inhibition or escape, intervention and therapy.Frontiers in cellular and infection microbiology · 2023Review
- Can pyroptosis be a new target in rheumatoid arthritis treatment?Frontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SARS-CoV-2 is a type of beta-CoV that develops acute pneumonia, which is an inflammatory condition. A cytokine storm has been recognized as one of the leading causes of death in patients with COVID-19. ALI and ARDS along with multiple organ failure have also been presented as the consequences of acute inflammation and cytokine storm. It has been previously confirmed that SARS-CoV, as another member of the beta-CoV family, activates NLRP3 inflammasome and consequently develops acute inflammation in a variety of ways through having complex interactions with the host immune system using structural and nonstructural proteins. Numerous studies conducted on Tranilast have further demonstrated that the given drug can act as an effective anti-chemotactic factor on controlling inflammation, and thus, it can possibly help the improvement of the acute form of COVID-19 by inhibiting some key inflammation-associated transcription factors such as NF-κB and impeding NLRP3 inflammasome. Several studies have comparably revealed the direct effect of this drug on the prevention of inappropriate tissue's remodeling; inhibition of neutrophils, IL-5, and eosinophils; repression of inflammatory cell infiltration into inflammation site; restriction of factors involved in acute airway inflammation like IL-33; and suppression of cytokine IL-13, which increase mucosal secretions. Therefore, Tranilast may be considered as a potential treatment for patients with the acute form of COVID-19 along with other drugs.
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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 Socratic graph.