Evidence map›Paper›PMID 37951043›Full record

ReviewDNA repair2024

Telomeres as hotspots for innate immunity and inflammation.

Joe Nassour, Sara Przetocka, Jan Karlseder

Open access · greenAbstract readReview
In one paragraph

Review in DNA repair, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.9field-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

26 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Telomere Crisis Shapes Cancer Evolution.Cold Spring Harbor perspectives in biology · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Observational
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review
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.

Joe NassourDepartment of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, 12801 E. 17th Ave, Aurora, CO 80045, USA; The Salk Institute for Biological Studies, 10010 North Torrey Pines Rd, La Jolla, CA 92037, USA.
Sara PrzetockaThe Salk Institute for Biological Studies, 10010 North Torrey Pines Rd, La Jolla, CA 92037, USA.
Jan KarlsederThe Salk Institute for Biological Studies, 10010 North Torrey Pines Rd, La Jolla, CA 92037, USA. Electronic address: karlseder@salk.edu.
Salk Institute for Biological Studies · US

Funding

Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Ye Zheng · 1985 to 2026
$82.8M
Understanding the role of autophagy-regulated cell death in the escape from replicative crisisR01CA234047 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI KARLSEDER, JAN, SHAW, REUBEN · 2020 to 2024
$3.1M
A nucleus-to-mitochondria nucleic acid-sensing pathway prevents bypass of age-associated proliferative boundariesR01AG077324 · NIA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Jan Karlseder · 2022 to 2026
$3.0M
Mitochondria-to-Nucleus Signaling in Colorectal CancerR01CA228211 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI HARGREAVES, DIANA CLARE, SHADEL, GERALD · 2020 to 2024
$2.6M
Understanding DNA break repair pathway choice regulation by the cNHEJ inhibitor CYRENR01CA227934 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI KARLSEDER, JAN · 2018 to 2022
$2.2M
The role of autophagy in the escape from replicative crisis and tumorigenesisR00CA252447 · NCI · UNIVERSITY OF COLORADO DENVER · PI NASSOUR, JOE · 2023 to 2025
$747k
The role of autophagy in the escape from replicative crisis and tumorigenesisK99CA252447 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI NASSOUR, JOE · 2020 to 2021
$326k
NCI NIH HHS K99 CA252447NCI NIH HHS P30 CA014195NCI NIH HHS R00 CA252447NCI NIH HHS R01 CA227934NCI NIH HHS R01 CA228211NCI NIH HHS R01 CA234047NIA NIH HHS R01 AG077324
6 · The paper itself

Abstract

Aging is marked by the gradual accumulation of deleterious changes that disrupt organ function, creating an altered physiological state that is permissive for the onset of prevalent human diseases. While the exact mechanisms governing aging remain a subject of ongoing research, there are several cellular and molecular hallmarks that contribute to this biological process. This review focuses on two factors, namely telomere dysfunction and inflammation, which have emerged as crucial contributors to the aging process. We aim to discuss the mechanistic connections between these two distinct hallmarks and provide compelling evidence highlighting the loss of telomere protection as a driver of pro-inflammatory states associated with aging. By reevaluating the interplay between telomeres, innate immunity, and inflammation, we present novel perspectives on the etiology of aging and its associated diseases.

Indexed as

AgingTelomereCellular SenescenceHumansImmunity, InnateInflammationAgingCancerGenome stabilityInflammationInnate immunityTelomeres

Identifiers

PMID37951043
PMCPMC10842095
OpenAlexW4388383236

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.