Evidence map›Paper›PMID 34445229›Full record

ReviewInternational journal of molecular sciences2021

Mitochondria-Induced Immune Response as a Trigger for Neurodegeneration: A Pathogen from Within.

Marta Luna-Sánchez, Patrizia Bianchi, Albert Quintana

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
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  7. Article
  8. Review
  9. Mitochondrial RNA in Inflammation.International journal of biological sciences · 2025
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Mitochondrial DNA and Inflammation in Alzheimer's Disease.Current issues in molecular biology · 2023
    Review
  17. Article
  18. Review
  19. Article
  20. Article
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 1 institution in 1 country.

Marta Luna-SánchezInstitut de Neurociències, Universitat Autònoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
Patrizia BianchiInstitut de Neurociències, Universitat Autònoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
Albert QuintanaInstitut de Neurociències, Universitat Autònoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
Universitat Autònoma de Barcelona · ES

Funding

Agència de Gestió d'Ajuts Universitaris i de Recerca 2017SGR-323"la Caixa" Foundation LCF/PR/HR20/52400018Ministerio de Ciencia e Innovación IJC2018-036938-IMinisterio de Economía, Industria y Competitividad, Gobierno de España SAF2014-57981PMinisterio de Economía, Industria y Competitividad, Gobierno de España SAF2017-88108-Rthe European Research Council ERC-2014-StG-638106
6 · The paper itself

Abstract

Symbiosis between the mitochondrion and the ancestor of the eukaryotic cell allowed cellular complexity and supported life. Mitochondria have specialized in many key functions ensuring cell homeostasis and survival. Thus, proper communication between mitochondria and cell nucleus is paramount for cellular health. However, due to their archaebacterial origin, mitochondria possess a high immunogenic potential. Indeed, mitochondria have been identified as an intracellular source of molecules that can elicit cellular responses to pathogens. Compromised mitochondrial integrity leads to release of mitochondrial content into the cytosol, which triggers an unwanted cellular immune response. Mitochondrial nucleic acids (mtDNA and mtRNA) can interact with the same cytoplasmic sensors that are specialized in recognizing genetic material from pathogens. High-energy demanding cells, such as neurons, are highly affected by deficits in mitochondrial function. Notably, mitochondrial dysfunction, neurodegeneration, and chronic inflammation are concurrent events in many severe debilitating disorders. Interestingly in this context of pathology, increasing number of studies have detected immune-activating mtDNA and mtRNA that induce an aberrant production of pro-inflammatory cytokines and interferon effectors. Thus, this review provides new insights on mitochondria-driven inflammation as a potential therapeutic target for neurodegenerative and primary mitochondrial diseases.

Indexed as

AnimalsCytokinesDNA, MitochondrialHumansMitochondriaNeurodegenerative DiseasesRNA, MitochondrialCytokinesDNA, MitochondrialRNA, Mitochondrialantiviral responseinflammationinnate immunityinterferonmitochondrial disordersmitochondrial dysfunctionmtDNAmtRNAneurodegeneration

Identifiers

PMID34445229
PMCPMC8395232
OpenAlexW3192075866

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.