Evidence map›Paper›PMID 36926349›Full record

ReviewFrontiers in immunology2023

cGAS-STING pathway as a potential trigger of immunosenescence and inflammaging.

Carine Raquel Richter Schmitz, Rafael Moura Maurmann, Fatima T C R Guma, Moisés Evandro Bauer, Florencia Maria Barbé-Tuana

Open access · goldFull text readReview
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
10.7field-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

61 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Bioactive materials · 2026
    Article
  7. Review
  8. Anti-aging effects of glycyrrhizin via maintaining Klotho levels.Journal of clinical biochemistry and nutrition · 2026
    Article
  9. Article
  10. Review
  11. Review
  12. Extracellular cGAMP in health and disease.Molecular biomedicine · 2026
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review

1 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

5 authors at 3 institutions in 1 country.

Carine Raquel Richter SchmitzLaboratório de Imunobiologia, Escola de Ciências da Saúde e da Vida, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.
Rafael Moura MaurmannLaboratório de Imunobiologia, Escola de Ciências da Saúde e da Vida, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.
Fatima T C R GumaPrograma de Pós-Graduação em Ciência Biológicas - Bioquímica, Departamento de Bioquímica, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Moisés Evandro BauerLaboratório de Imunobiologia, Escola de Ciências da Saúde e da Vida, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.
Florencia Maria Barbé-TuanaLaboratório de Imunobiologia, Escola de Ciências da Saúde e da Vida, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.
Pontifícia Universidade Católica do Rio Grande do Sul · BRNational Council for Scientific and Technological Development · BRUniversidade Federal do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is associated with an increased incidence of autoimmune diseases, despite the progressive decline of immune responses (immunosenescence). This apparent paradox can be explained by the age-related chronic low-grade systemic inflammation (inflammaging) and progressive dysregulation of innate signaling. During cellular aging, there is an accumulation of damaged DNA in the cell's cytoplasm, which serves as ubiquitous danger-associated molecule, promptly recognized by DNA sensors. For instance, the free cytoplasmic DNA can be recognized, by DNA-sensing molecules like cGAS-STING (cyclic GMP-AMP synthase linked to a stimulator of interferon genes), triggering transcriptional factors involved in the secretion of pro-inflammatory mediators. However, the contribution of this pathway to the aging immune system remains largely unknown. Here, we highlight recent advances in understanding the biology of the cGAS-STING pathway, its influence on the senescence-associated secretory phenotype (SASP), and its modulation of the immune system during sterile inflammation. We propose that this important stress sensor of DNA damage is also a trigger of immunosenescence and inflammaging.

Indexed as

ImmunosenescenceCellular SenescenceDNAHumansInflammationNucleotidyltransferasesDNANucleotidyltransferasesagingcGASimmunosenescenceinflammagingNF-κBSASPsenescence

Identifiers

PMID36926349
PMCPMC10011111
OpenAlexW4323320144

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read1
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.