Evidence map›Paper›PMID 25330206›Full record

ReviewAntioxidants & redox signaling2015

Redox regulation of NLRP3 inflammasomes: ROS as trigger or effector?

Justine M Abais, Min Xia, Yang Zhang, Krishna M Boini, Pin-Lan Li

Open access · hybridAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 495 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
495citing papers in PubMed, 2 pooled it
11.8field-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

495 citing papers in PubMed, 2 syntheses or guidelines pooled it, 908 citations in OpenAlex.

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  20. From Glycocalyx Shedding to Microvascular Collapse in Sepsis: Endothelial Pathophysiology, Organ Dysfunction, and Mechanistic Biomarkers.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review

435 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Justine M AbaisDepartment of Pharmacology and Toxicology, Virginia Commonwealth University , Richmond, Virginia.
Min Xia
Yang Zhang
Krishna M Boini
Pin-Lan Li
Virginia Commonwealth University · US

Funding

Regulation of Lysosomes in Autophagy in Coronary Arterial MyocytesR01HL057244 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2001 to 2021
$6.7M
Subendothelial Exosomes in Coronary Microvascular DysfunctionR01HL075316 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2004 to 2024
$6.7M
Hypertension and glomerular injury in hyperhomocysteinemia - role of inflammatory exosomesR01DK054927 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 1998 to 2023
$6.7M
Lysosome dysfunction in podocytopathy and associated hypertensionR01DK120491 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2018 to 2022
$2.4M
NAADP-Sensitive Lysosomal Ca2+ Release Channels-TRP-ML1 in Arterial MyocytesR01HL091464 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2009 to 2013
$2.2M
MECHANISM OF CORONARY ENDOTHELIUM MEDIATED VASODILATIONR29HL057244 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI LI, PIN-LAN · 1997 to 2000
$101k
Redox Triggering of Glomerular NALP3 Inflammasomes in HyperhomocysteinemiaF31AG043289 · NIA · VIRGINIA COMMONWEALTH UNIVERSITY · PI ABAIS-BATTAD, JUSTINE M · 2012 to 2013
$64k
NHLBI NIH HHS HL075316NHLBI NIH HHS HL091464NHLBI NIH HHS HL57244NHLBI NIH HHS R01 HL057244NHLBI NIH HHS R01 HL075316NIA NIH HHS 1F31AG043289-01NIDDK NIH HHS DK54927NIDDK NIH HHS R01 DK054927NIDDK NIH HHS R01 DK120491
6 · The paper itself

Abstract

significanceInflammasomes are multiprotein complexes localized within the cytoplasm of the cell that are responsible for the maturation of proinflammatory cytokines such as interleukin-1β (IL-1β) and IL-18, and the activation of a highly inflammatory form of cell death, pyroptosis. In response to infection or cellular stress, inflammasomes are assembled, activated, and involved in host defense and pathophysiology of diseases. Clarification of the molecular mechanisms leading to the activation of this intracellular inflammatory machinery may provide new insights into the concept of inflammation as the root of and route to human diseases. RECENT ADVANCES: The activation of inflammasomes, specifically the most fully characterized inflammasome-the nucleotide-binding oligomerization domain (NOD)-like receptor containing pyrin domain 3 (NLRP3) inflammasome, is now emerging as a critical molecular mechanism for many degenerative diseases. Several models have been developed to describe how NLRP3 inflammasomes are activated, including K(+) efflux, lysosome function, endoplasmic reticulum (ER) stress, intracellular calcium, ubiquitination, microRNAs, and, in particular, reactive oxygen species (ROS). CRITICAL ISSUES: ROS may serve as a "kindling" or triggering factor to activate NLRP3 inflammasomes as well as "bonfire" or "effector" molecules, resulting in pathological processes. Increasing evidence seeks to understand how this spatiotemporal action of ROS occurs during NLRP3 inflammasome activation, which will be a major focus of this review. FUTURE DIRECTIONS: It is imperative to know how this dual action of ROS works during NLRP3 inflammation activation on different stimuli and what relevance such spatiotemporal redox regulation of NLRP3 inflammasomes has in cell or organ functions and possible human diseases.

Indexed as

AnimalsCarrier ProteinsEndoplasmic Reticulum StressHumansInflammasomesInflammationLysosomesMitochondriaNeurodegenerative DiseasesNLR Family, Pyrin Domain-Containing 3 ProteinOxidation-ReductionReactive Oxygen SpeciesUnfolded Protein ResponseCarrier ProteinsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanReactive Oxygen Species

Identifiers

PMID25330206
PMCPMC4403231
OpenAlexW2077549620

What OpenQuestion holds

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Registered trials

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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.