Evidence map›Paper›PMID 29221810›Full record

ReviewMitochondrion2018

Mitochondrial dysfunction and damage associated molecular patterns (DAMPs) in chronic inflammatory diseases.

Charles S Dela Cruz, Min-Jong Kang

Open access · greenAbstract readReview
In one paragraph

Review in Mitochondrion, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

128 citing papers in PubMed, 234 citations in OpenAlex.

  1. Article
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  4. Review
  5. Dual role of homocysteine in enhancing metabolic activity and suppressing inflammatory cytokines in murine immune cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
  6. Review
  7. Article
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  9. 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
  10. Article
  11. Review
  12. Relationship between different modes of death and premature ovarian insufficiency: a literature review.Apoptosis : an international journal on programmed cell death · 2026
    Review
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68 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 1 institution in 1 country.

Charles S Dela CruzSection of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520-8057, United States. Electronic address: Charles.delacruz@yale.edu.
Min-Jong KangSection of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520-8057, United States. Electronic address: min-jong.kang@yale.edu.
Yale University · US

Funding

Host-Pneumococcal Interaction in the LungR01HL126094 · NHLBI · YALE UNIVERSITY · PI DELA CRUZ, CHARLES S · 2015 to 2019
$2.1M
The reduction of NLRX1 and its role in pulmonary agingR01AG053495 · NIA · YALE UNIVERSITY · PI KANG, MIN-JONG · 2016 to 2020
$1.7M
Role of NLRX1 in cigarette smoke-induced pulmonary inflammation and remodelingR01HL130283 · NHLBI · YALE UNIVERSITY · PI KANG, MIN-JONG · 2016 to 2019
$1.7M
NHLBI NIH HHS R01 HL126094NHLBI NIH HHS R01 HL130283NIA NIH HHS R01 AG053495
6 · The paper itself

Abstract

Inflammation represents a comprehensive host response to external stimuli for the purpose of eliminating the offending agent, minimizing injury to host tissues and fostering repair of damaged tissues back to homeostatic levels. In normal physiologic context, inflammatory response culminates with the resolution of infection and tissue damage response. However, in a pathologic context, persistent or inappropriately regulated inflammation occurs that can lead to chronic inflammatory diseases. Recent scientific advances have integrated the role of innate immune response to be an important arm of the inflammatory process. Accordingly, the dysregulation of innate immunity has been increasingly recognized as a driving force of chronic inflammatory diseases. Mitochondria have recently emerged as organelles which govern fundamental cellular functions including cell proliferation or differentiation, cell death, metabolism and cellular signaling that are important in innate immunity and inflammation-mediated diseases. As a natural consequence, mitochondrial dysfunction has been highlighted in a myriad of chronic inflammatory diseases. Moreover, the similarities between mitochondrial and bacterial constituents highlight the intrinsic links in the innate immune mechanisms that control chronic inflammation in diseases where mitochondrial damage associated molecular patterns (DAMPs) have been involved. Here in this review, the role of mitochondria in innate immune responses is discussed and how it pertains to the mitochondrial dysfunction or DAMPs seen in chronic inflammatory diseases is reviewed.

Indexed as

AlarminsAnimalsChronic DiseaseHumansInflammationMitochondriaMitochondrial DiseasesMitochondrial ProteinsAlarminsMitochondrial ProteinsChronic inflammationDAMPsInnate immunityMitochondria

Identifiers

PMID29221810
PMCPMC5988941
OpenAlexW2771620838

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.