Evidence map›Paper›PMID 27538510›Full record

ReviewCurrent drug targets2017

Inflammasome Activation in Chronic Glomerular Diseases.

Sabena M Conley, Justine M Abais, Krishna M Boini, Pin-Lan Li

Open access · greenAbstract readReview
In one paragraph

Review in Current drug targets, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Sabena M ConleyDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, School of Medicine, Richmond, VA, 23298. United States.
Justine M AbaisDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, School of Medicine, Richmond, VA, 23298. United States.
Krishna M BoiniDepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX, 77204. United States.
Pin-Lan LiDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, School of Medicine, Richmond, VA, 23298. United States.
Virginia Commonwealth University · USUniversity of Houston · US

Funding

Regulation of Lysosomes in Autophagy in Coronary Arterial MyocytesR01HL057244 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2001 to 2021
$6.7M
Hypertension and glomerular injury in hyperhomocysteinemia - role of inflammatory exosomesR01DK054927 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 1998 to 2023
$6.7M
Virginia Commonwealth University Initiative for Maximizing Student DevelopmentR25GM090084 · NIGMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI AKBARALI, HAMID I, LLOYD, JOYCE A. · 2010 to 2022
$5.2M
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
Instigation of Glomerular Injury by Inflammasomes in Obesity: Beyond InflammationR01DK104031 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI BOINI, KRISHNA M · 2015 to 2019
$1.7M
MECHANISM OF CORONARY ENDOTHELIUM MEDIATED VASODILATIONR29HL057244 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI LI, PIN-LAN · 1997 to 2000
$101k
NHLBI NIH HHS R01 HL057244NHLBI NIH HHS R01 HL091464NHLBI NIH HHS R29 HL057244NIDDK NIH HHS R01 DK054927NIDDK NIH HHS R01 DK104031NIDDK NIH HHS R01 DK120491NIGMS NIH HHS R25 GM090084
6 · The paper itself

Abstract

backgroundThe intracellular multiprotein complex termed the inflammasome functions as a platform of pro-inflammatory cytokine production such as IL-1β and IL-18. Under certain conditions, however, the inflammasome produces non-canonical effects such as induction of cell death, pyroptosis and cell metabolism alterations.

objectiveIn mammalian cells, several types of inflammasomes were identified, but the most widely studied one is the inflammasome containing NOD-like receptor with pyrin domain 3 (NLRP3), which has recently been reported as a central pathogenic mechanism of chronic degenerative diseases. Many activators or risk factors exert their actions through the activation of the NLRP3 inflammasome to produce a variety of functional changes in different cells including inflammatory, metabolic or survival responses. Several molecular signaling pathways are shown to mediate the activation of the NLRP3 inflammasome, and they are related to the modifications in K+ efflux, increased lysosome leakage and activation of cathepsin B or enhanced reactive oxygen species (ROS) production. In the kidney, inflammation is believed to mediate or promote the progression of glomerular sclerotic pathologies resulting in end-stage renal disease (ESRD). NLRP3 inflammasome activation may turn on glomerular inflammation and other cell damages, contributing to the onset of glomerular injury and ESRD. This inflammasome activation not only occurs in immune cells, but also in residential cells such as endothelial cells and podocytes in the glomeruli. SUMMARY: This review briefly summarizes current evidence of NLRP3 inflammasome activation and related molecular mechanisms in renal glomeruli. The possible canonical and non-canonical effects of this inflammasome activation and its potential implication in the development of different glomerular diseases are highlighted.

Indexed as

Chronic DiseaseGlomerulonephritisHumansInflammasomesKidney GlomerulusNLR Family, Pyrin Domain-Containing 3 ProteinInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humandiabetes mellitusglomerulosclerosishomocysteineinflammasomeInflammation

Identifiers

PMID27538510
PMCPMC5893309
OpenAlexW2517290330

What OpenQuestion holds

Textmetadata
LicenceTDM
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.