Evidence map›Paper›PMID 26067258›Full record

ArticleAntioxidants & redox signaling2015

The Roles of Mitochondrial Damage-Associated Molecular Patterns in Diseases.

Kiichi Nakahira, Shu Hisata, Augustine M K Choi

Registry-linked trialAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03539497 (Prognostic Value of Plasma Mitochondrial DNA and Cytochrome C After Cardiac Arrest), which is not on this map. Cited by 204 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
204citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% 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.

NCT03539497 unknown statusnot on this mapstarted 2019, after this paper: background citation

Prognostic Value of Plasma Mitochondrial DNA and Cytochrome C After Cardiac Arrest

TypeobservationalSponsorUniversity Medical Centre LjubljanaRan2019 to 2024Enrolled87ConditionsCardiac ArrestArmsBiomarker
3 · Its place in the literature

Who cites it

204 citing papers in PubMed, 1 synthesis or guideline pooled it, 339 citations in OpenAlex.

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144 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 at 2 institutions in 1 country.

Kiichi Nakahira1 Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College and New York-Presbyterian Hospital , New York, New York.
Shu Hisata1 Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College and New York-Presbyterian Hospital , New York, New York.
Augustine M K Choi1 Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College and New York-Presbyterian Hospital , New York, New York.
Cornell University · USPresbyterian Hospital · US

Funding

The Role of HEME Oxygenase in Hyperoxic Lung InjuryR01HL055330 · NHLBI · YALE UNIVERSITY · PI CHOI, AUGUSTINE M, CHOI, MARY E · 1998 to 2021
$6.6M
HEME OXYGENASE 1--LUNG VASCULAR CELL HYPOXIC RESPONSER01HL060234 · NHLBI · YALE UNIVERSITY · PI CHOI, AUGUSTINE M, CHOI, MARY E · 1999 to 2017
$5.8M
NHLBI NIH HHS R01 HL055330NHLBI NIH HHS R01 HL060234
6 · The paper itself

Abstract

significanceMitochondria, vital cellular power plants to generate energy, are involved in immune responses. Mitochondrial damage-associated molecular patterns (DAMPs) are molecules that are released from mitochondria to extracellular space during cell death and include not only proteins but also DNA or lipids. Mitochondrial DAMPs induce inflammatory responses and are critically involved in the pathogenesis of various diseases. RECENT ADVANCES: Recent studies elucidate the molecular mechanisms by which mitochondrial DAMPs are released and initiate immune responses by use of genetically modulated cells or animals. Importantly, the levels of mitochondrial DAMPs in patients are often associated with severity and prognosis of human diseases, such as infection, asthma, ischemic heart disease, and cancer. CRITICAL ISSUES: Although mitochondrial DAMPs can represent proinflammatory molecules in various experimental models, their roles in human diseases may be multifunctional and complex. It remains unclear where and how mitochondrial DAMPs are liberated into extracellular spaces and exert their biological functions particularly in vivo. In addition, while mitochondria can secrete several types of DAMPs during cell death, the interaction of each mitochondrial DAMP (e.g., synergistic effects) remains unclear. FUTURE DIRECTIONS: Regulation of mitochondrial DAMP-mediated immune responses may be important to alter the progression of human diseases. In addition, measuring mitochondrial DAMPs in patients may be clinically useful as biomarkers to predict prognosis or response to therapies. Further studies of the mechanisms by which mitochondrial DAMPs impact the initiation and progression of diseases may lead to the development of therapeutics specifically targeting this pathway. Antioxid.

Indexed as

AnimalsDNA, MitochondrialExtracellular SpaceHumansInflammationMitochondriaMitochondrial ProteinsSignal TransductionDNA, MitochondrialMitochondrial Proteins

Identifiers

PMID26067258
PMCPMC4685486
OpenAlexW1783831484

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.