Evidence map›Paper›PMID 37081238›Full record

ReviewCellular and molecular life sciences : CMLS2023

Aging microglia.

Ignazio Antignano, Yingxiao Liu, Nina Offermann, Melania Capasso

Abstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

70 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Oxytocin as regulator of stress and inflammation in aging.Neuroscience and biobehavioral reviews · 2026
    Review
  4. Article
  5. Article
  6. miR-214-3p and NCKAP1: A microglial functional dimension of Alzheimer's progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Alkaloids from In Vitro CulturedPlants (Basel, Switzerland) · 2026
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

10 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

4 authors.

Ignazio AntignanoDeutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Bonn, Germany.
Yingxiao LiuDeutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Bonn, Germany.
Nina OffermannDeutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Bonn, Germany.
Melania CapassoDeutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Bonn, Germany. melania.capasso@dzne.de.ORCID http://orcid.org/0000-0001-8659-9867

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia are the tissue-resident macrophage population of the brain, specialized in supporting the CNS environment and protecting it from endogenous and exogenous insults. Nonetheless, their function declines with age, in ways that remain to be fully elucidated. Given the critical role played by microglia in neurodegenerative diseases, a better understanding of the aging microglia phenotype is an essential prerequisite in designing better preventive and therapeutic strategies. In this review, we discuss the most recent literature on microglia in aging, comparing findings in rodent models and human subjects.

Indexed as

MicrogliaAgingAnimalsBrain-Gut AxisCellular SenescenceHumansMonocytesOxidative StressSignal TransductionAgingHuman microgliaMicrogliaNeuroinflammationRNAseqSenescence

Identifiers

PMID37081238
PMCPMC10119228

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.