ReviewTanaffos2023
Involvement of NLRP3 Inflammasome in SARS-Cov-2-Induced Multiorgan Dysfunction in Patients with COVID-19: A Review of Molecular Mechanisms.
Review in Tanaffos, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed, 0 citations in OpenAlex.
- The NLRP3 inflammasome as a key pathway in the affective and chronic fatigue symptoms of Long COVID.Journal of translational medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleotide-binding domain and leucine-rich repeat protein- 3 (NLRP3) inflammasome is a critical component of the innate immune system. The inflammasome activation is correlated with the COVID- 19 severity. Furthermore, the underlying conditions are accompanied by hyperactivation of NLRP3 inflammasome and poor outcomes. Herein, we presented the involvement of NLRP3 inflammasome in the pathogenies of SARS-CoV-2-induced multiorgan dysfunction and potential therapeutics. Overexpression of NLRP3 inflammasome components and subsequently increased levels of cytokines following viral infection leads to the cytokine storm and indirectly affects the organ functions. Besides, invading host cells via SARS-CoV-2 further activates the NLRP3 inflammasome and induces pyroptosis in immune cells, resulting in the secretion of higher levels of proinflammatory cytokines into the extracellular matrix. These events continued by induction of fibrosis and organ dysfunction following infection with SARS-CoV-2 in critically ill patients. This condition can be observed in individuals with comorbidities (e.g., diabetes, obesity, etc.) due to a primed state of immunity, which can cause severe disease or death in this population. Therefore, understanding the mechanisms underlying host-SARS-CoV-2 interaction may help to clarify the pathophysiology of SARS-CoV-2- induced multiorgan dysfunction and introduce potential therapeutic strategies.
Indexed as
Identifiers
37920322PMC10618576W4388302476What Socratic holds
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.