Evidence map›Paper›PMID 37001140›Full record

ReviewAnnual review of biochemistry2023

Mitochondrial DNA Release in Innate Immune Signaling.

Laura E Newman, Gerald S Shadel

Open access · hybridAbstract readReview
In one paragraph

Review in Annual review of biochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
189citing papers in PubMed, 3 pooled it
38.3field-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

189 citing papers in PubMed, 3 syntheses or guidelines pooled it, 233 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
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  7. Mitophagy coordinates organelle crosstalk in health and diseases.Signal transduction and targeted therapy · 2026
    Review
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  11. Article
  12. The Hallmarks of Aging: From Molecular Mechanisms to Clinical Translation.International journal of molecular sciences · 2026
    Review
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  18. Article
  19. YBX1 regulates RNA polymerase III transcripts to prevent inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  20. Review

129 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.

Laura E NewmanSalk Institute for Biological Studies, La Jolla, California, USA; email: gshadel@salk.edu.
Gerald S ShadelSalk Institute for Biological Studies, La Jolla, California, USA; email: gshadel@salk.edu.
Salk Institute for Biological Studies · US

Funding

San Diego Nathan Shock CenterP30AG068635 · NIA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI METALLO, CHRISTIAN MICHAEL · 2020 to 2024
$6.0M
Mitochondrial DNA Stress Activation of Interferon Signaling and Lupus PathologyR01AR069876 · NIAMS · YALE UNIVERSITY · PI SHADEL, GERALD · 2017 to 2021
$2.1M
The role of mitochondrial/ER contacts in the regulation of mtDNA release from mitochondria, innate immune signaling, and responses to viral infectionK99GM141482 · NIGMS · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI NEWMAN, LAURA ELIZABETH · 2021 to 2022
$200k
NIAMS NIH HHS R01 AR069876NIA NIH HHS P30 AG068635NIGMS NIH HHS K99 GM141482
6 · The paper itself

Abstract

According to the endosymbiotic theory, most of the DNA of the original bacterial endosymbiont has been lost or transferred to the nucleus, leaving a much smaller (∼16 kb in mammals), circular molecule that is the present-day mitochondrial DNA (mtDNA). The ability of mtDNA to escape mitochondria and integrate into the nuclear genome was discovered in budding yeast, along with genes that regulate this process. Mitochondria have emerged as key regulators of innate immunity, and it is now recognized that mtDNA released into the cytoplasm, outside of the cell, or into circulation activates multiple innate immune signaling pathways. Here, we first review the mechanisms through which mtDNA is released into the cytoplasm, including several inducible mitochondrial pores and defective mitophagy or autophagy. Next, we cover how the different forms of released mtDNA activate specific innate immune nucleic acid sensors and inflammasomes. Finally, we discuss how intracellular and extracellular mtDNA release, including circulating cell-free mtDNA that promotes systemic inflammation, are implicated in human diseases, bacterial and viral infections, senescence and aging.

Indexed as

DNA, MitochondrialMitochondriaAgingAnimalsCell NucleusHumansImmunity, InnateMammalsDNA, MitochondrialdiseaseDNA sensinginflammationmitochondriapore

Identifiers

PMID37001140
PMCPMC11058562
OpenAlexW4362459424

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.