Evidence map›Paper›PMID 37520548›Full record

ReviewFrontiers in immunology2023

NLRP3: a new therapeutic target in alcoholic liver disease.

Subhashini Brahadeeswaran, Tiasha Dasgupta, Venkatraman Manickam, Viswanathan Saraswathi, Ramasamy Tamizhselvi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

27 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Alcohol-related liver disease.Gastroenterology report · 2025
    Review
  15. Pharmacotherapy of Liver Fibrosis and Hepatitis: Recent Advances.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
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 2 institutions in 2 countries.

Subhashini BrahadeeswaranDepartment of Biosciences, School of Biosciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu, India.
Tiasha DasguptaDepartment of Biosciences, School of Biosciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu, India.
Venkatraman ManickamDepartment of Biosciences, School of Biosciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu, India.
Viswanathan SaraswathiDepartment of Internal Medicine, Division of Diabetes, Endocrinology, and Metabolism, Veterans Affairs Medical Center, University of Nebraska Medical Center, Omaha, NE, United States.
Ramasamy TamizhselviDepartment of Biosciences, School of Biosciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu, India.
Vellore Institute of Technology University · INUniversity of Nebraska Medical Center · US

Funding

The Role of TP-R on Alcohol-Induced Multi-Organ Damage: Liver and HeartP50AA030407 · NIAAA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Kusum K. Kharbanda · 2023 to 2026
$7.9M
TP-R: a novel mediator of obesity-linked insulin resistance in humansI01CX002084 · VA · OMAHA VA MEDICAL CENTER · PI DESOUZA, CYRUS V, VISWANATHAN, SARASWATHI · 2021 to 2025
–
CSRD VA I01 CX002084NIAAA NIH HHS P50 AA030407
6 · The paper itself

Abstract

The liver is in charge of a wide range of critical physiological processes and it plays an important role in activating the innate immune system which elicits the inflammatory events. Chronic ethanol exposure disrupts hepatic inflammatory mechanism and leads to the release of proinflammatory mediators such as chemokines, cytokines and activation of inflammasomes. The mechanism of liver fibrosis/cirrhosis involve activation of NLRP3 inflammasome, leading to the destruction of hepatocytes and subsequent metabolic dysregulation in humans. In addition, increasing evidence suggests that alcohol intake significantly modifies liver epigenetics, promoting the development of alcoholic liver disease (ALD). Epigenetic changes including histone modification, microRNA-induced genetic modulation, and DNA methylation are crucial in alcohol-evoked cell signaling that affects gene expression in the hepatic system. Though we are at the beginning stage without having the entire print of epigenetic signature, it is time to focus more on NLRP3 inflammasome and epigenetic modifications. Here we review the novel aspect of ALD pathology linking to inflammation and highlighting the role of epigenetic modification associated with NLRP3 inflammasome and how it could be a therapeutic target in ALD.

Indexed as

InflammasomesLiver Diseases, AlcoholicFibrosisHepatocytesHumansLiver CirrhosisNLR Family, Pyrin Domain-Containing 3 ProteinInflammasomesNLR Family, Pyrin Domain-Containing 3 Proteinalcoholalcohol liver diseaseepigeneticsinterleukin 18interleukin 1βNLRP3 inflammasomepro-caspase-1pyroptosis

Identifiers

PMID37520548
PMCPMC10374212
OpenAlexW4384155362

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.