Evidence map›Paper›PMID 30165038›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2018

Mitochondria in innate immune signaling.

Balaji Banoth, Suzanne L Cassel

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 238 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
238citing papers in PubMed, 1 pooled it
10.7field-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

238 citing papers in PubMed, 1 synthesis or guideline pooled it, 401 citations in OpenAlex.

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178 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

2 authors at 2 institutions in 1 country.

Balaji BanothWomen's Guild Lung Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Suzanne L CasselWomen's Guild Lung Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California. Electronic address: suzanne.cassel@cshs.org.
Cedars-Sinai Medical Center · USLung Institute · US

Funding

Mechanisms of NIrp3 inflammasome activation by mitochondrial dysfunctionR01AI104706 · NIAID · UNIVERSITY OF IOWA · PI CASSEL, SUZANNE L. · 2014 to 2018
$2.1M
NIAID NIH HHS R01 AI104706
6 · The paper itself

Abstract

Mitochondria are functionally versatile organelles. In addition to their conventional role of meeting the cell's energy requirements, mitochondria also actively regulate innate immune responses against infectious and sterile insults. Components of mitochondria, when released or exposed in response to dysfunction or damage, can be directly recognized by receptors of the innate immune system and trigger an immune response. In addition, despite initiation that may be independent from mitochondria, numerous innate immune responses are still subject to mitochondrial regulation as discrete steps of their signaling cascades occur on mitochondria or require mitochondrial components. Finally, mitochondrial metabolites and the metabolic state of the mitochondria within an innate immune cell modulate the precise immune response and shape the direction and character of that cell's response to stimuli. Together, these pathways result in a nuanced and very specific regulation of innate immune responses by mitochondria.

Indexed as

Immunity, InnateSignal TransductionAlarminsAnimalsDNA, MitochondrialHumansMitochondriaModels, BiologicalAlarminsDNA, MitochondrialASC, Apoptosis Associated Speck like protein containing CARDASK1, apoptosis signal-regulating kinase 1ATP, adenosine tri-phosphateCAPS, cryopyrin associated periodic syndromesCARD, caspase activation and recruitment domainCgas, cyclic GMP-AMP synthaseCL, cardiolipinCLR, C-type lectin receptorCREB, cAMP response element binding proteinDAMP, damage associated molecular patternESCIT, evolutionarily conserved signaling intermediate in the toll pathwayETC, electron transport chainfMet, N-formylated methionineFPR, formyl peptide receptorHIF, hypoxia-inducible factorHMGB1, high mobility group box protein 1IFN, interferonIL, interleukinIRF, interferon regulatory factorJNK, cJUN NH2-terminal kinaseLPS, lipopolysaccharideLRR, leucine rich repeatMAPK, mitogen-activated protein kinaseMARCH5, membrane-associated ring finger (C3HC4) 5MAVS, mitochondrial antiviral signalingMAVS, mitochondrial antiviral signaling proteinMFN1/2, mitofusinMOMP, mitochondrial outer membrane permeabilizationMPT, mitochondrial permeability transitionmROS, mitochondrial ROSmtDNA, mitochondrial DNAMyD88, myeloid differentiation primary response 88NADH, nicotinamide adenine dinucleotideNBD, nucleotide binding domainn-fp, n-formyl peptidesNFκB, Nuclear factor κ BNLR, NOD like receptorNOD, nucleotide-binding oligomerization domainNRF2, nuclear factor erythroid 2-related factor 2PAMP, pathogen associated molecular patternPPAR, peroxisome proliferator-accelerated receptorPRRs, pathogen recognition receptorsRIG-I, retinoic acid inducible gene IRLR, retinoic acid inducible gene like receptorROS, reactive oxygen speciesSTING, stimulator of interferon geneTAK1, transforming growth factor-β-activated kinase 1TANK, TRAF family member-associated NFκB activatorTBK1, TANK Binding Kinase 1TCA, Tri-carboxylic acidTFAM, mitochondrial transcription factor ATLR, Toll Like ReceptorTRAF6, tumor necrosis factor receptor-associated factor 6TRIF, TIR-domain-containing adapter-inducing interferon βTUFM, Tu translation elongation factor.

Identifiers

PMID30165038
PMCPMC6218307
OpenAlexW2887324910

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.