Cited by 255Immune Response and InflammationInflammasome and immune disordersMitochondrial Function and Pathology

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

Open access
Dela Cruz, Charles S., Kang, Min-Jong·2018·Mitochondrion

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.

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Crossref · 10.1016/j.mito.2017.12.001

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  • In AD, chronic release of DAMPs, mitochondrial DAMPs, and pro-inflammatory molecules contributes to onset and progression of neurodegeneration.

    “in AD, the chronic release of DAMPs, mitochondrial-released DAMPs and pro-inflammatory molecules contributes to the onset and progression of neurodegeneration [57, 76, 97, 149, 194, 270, 304, 333, 345]”

    From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [76]

    Section III.E (page unavailable) includes Alzheimer’s disease among neurodegenerative disorders with neuroinflammation and says neuroinflammation and mitochondrial impairment may reinforce one another and ultimately lead to neuronal death. Section II.C describes mitochondrial DAMPs as potential drivers of inflammatory responses. The paper does not establish that chronic release of DAMPs and pro-inflammatory molecules contributes specifically to the onset and progression of neurodegeneration in Alzheimer’s disease; Section III.E cautions that neuroinflammation’s pathogenic role is difficult to define. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Mitochondrial dysfunction is a hallmark of many chronic inflammatory diseases, including diseases caused by the innate immune response.

    “Mitochondrial dysfunction is a hallmark of many chronic inflammatory diseases193, including those caused by the innate immune response194.”

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  1. Kumar VAA Aster JC 2015 Infalmmation and Repair, Robbins and Cotran Pathologic Basis of Disease 9 Saunders Philadelphia PA 69 111

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Authors
Dela Cruz, C. S., & Kang, M.-J.
Affiliations
Yale University (US)
Corresponding author
Kang, Min-Jong
Venue
Mitochondrion
Publisher
Elsevier BV
Published
2018-07
Volume
41
Pages
37-44
ISSN
1567-7249 (ISSN-L)
OpenAlex
W2771620838
Cited by
255
References
107
Citations by year
2026: 34 · 2025: 28 · 2024: 45 · 2023: 37 · 2022: 23 · 2021: 43 · 2020: 22 · 2019: 19 · 2018: 4
FWCI
1.27
Type
journal article
Language
en
Open access
Locations
  • Mitochondrion (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • NHLBI (R01HL130283, R01HL126094)
  • NIA (R01AG053495)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
mitochondrial dysfunction, damage-associated molecular patterns, chronic inflammatory diseases, innate immunity, mitochondrial DAMPs, mitochondrial signaling, mitochondrial metabolism, mitochondrial cell death
MeSH terms
Alarmins, Animals, Chronic Disease, Humans, Inflammation, Mitochondria, Mitochondrial Proteins, Mitochondrial Diseases

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