Evidence map›Paper›PMID 27439607›Full record

ReviewBMB reports2016

Mitophagy: a balance regulator of NLRP3 inflammasome activation.

Min-Ji Kim, Joo-Heon Yoon, Ji-Hwan Ryu

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in BMB reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

116 citing papers in PubMed, 1 synthesis or guideline pooled it.

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56 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

3 authors.

Min-Ji KimResearch Center for Natural Human Defense System, Brain Korea 21 PLUS Project for Medical Science, and Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul 03722, Korea.
Joo-Heon YoonResearch Center for Natural Human Defense System, Brain Korea 21 PLUS Project for Medical Science, Department of Otorhinolaryngology, and The Airway Mucus Institute, Yonsei University College of Medicine, Seoul 03722, Korea.
Ji-Hwan RyuBrain Korea 21 PLUS Project for Medical Science and Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul 03722, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NLRP3 inflammasome is activated by a variety of external or host-derived stimuli and its activation initiates an inflammatory response through caspase-1 activation, resulting in inflammatory cytokine IL-1β maturation and secretion. The NLRP3 inflammasome activation is a kind of innate immune response, most likely mediated by myeloid cells acting as a host defense mechanism. However, if this activation is not properly regulated, excessive inflammation induced by overactivated NLRP3 inflammasome can be detrimental to the host, causing tissue damage and organ dysfunction, eventually causing several diseases. Previous studies have suggested that mitochondrial damage may be a cause of NLRP3 inflammasome activation and autophagy, which is a conserved self-degradation process that negatively regulates NLRP3 inflammasome activation. Recently, mitochondria-selective autophagy, termed mitophagy, has emerged as a central player for maintaining mitochondrial homeostasis through the elimination of damaged mitochondria, leading to the prevention of hyperinflammation triggered by NLRP3 inflammasome activation. In this review, we will first focus on the molecular mechanisms of NLRP3 inflammasome activation and NLRP3 inflammasome-related diseases. We will then discuss autophagy, especially mitophagy, as a negative regulator of NLPP3 inflammasome activation by examining recent advances in research. [BMB Reports 2016; 49(10): 529-535].

Indexed as

MitophagyAutophagyHumansInflammasomesInterleukin-1betaMetabolic DiseasesMitochondriaNLR Family, Pyrin Domain-Containing 3 ProteinSepsisInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 Protein

Identifiers

PMID27439607
PMCPMC5227293

What OpenQuestion holds

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LicenceCC BY-NC
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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.