Evidence map›Paper›PMID 33906678›Full record

ReviewCell & bioscience2021

Galectin-3: a key player in microglia-mediated neuroinflammation and Alzheimer's disease.

Yinyin Tan, Yanqun Zheng, Daiwen Xu, Zhanfang Sun, Huan Yang, Qingqing Yin

Open access · goldAbstract readReview
In one paragraph

Review in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Pleiotropic regulatory mechanisms and targeted therapeutic prospects of Galectin-3 in aging-related diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  12. Review
  13. Article
  14. Review
  15. Microglial galectin-3 increases with aging in the mouse hippocampus.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

6 authors at 3 institutions in 1 country.

Yinyin TanDepartment of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, China.
Yanqun ZhengDepartment of Neurology, The Dongshan Hospital of Linyi, Linyi, 276017, Shandong, China.
Daiwen XuDepartment of Neurology, The People Hospital of Huaiyin Jinan, Jinan, 250021, Shandong, China.
Zhanfang SunDepartment of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, China.
Huan YangDepartment of Radiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, China.
Qingqing YinDepartment of Geriatric Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, China. yinyunqing11@126.com.ORCID http://orcid.org/0000-0003-0534-7436
Shandong Provincial Hospital · CNFourth People’s Hospital of Jinan · CNLinyi People's Hospital · CN

Funding

Jinan Science and Technology Bureau (CN) 201805073National Natural Science Foundation of China 82000771Natural Science Foundation of Shandong Province ZR2019PH017Project funded by China Postdoctoral Science Foundation 2017M622217Shandong Provincial Key Research and Development Project 2017G006008
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common cause of dementia and is characterized by the deposition of extracellular aggregates of amyloid-β (Aβ), the formation of intraneuronal tau neurofibrillary tangles and microglial activation-mediated neuroinflammation. One of the key molecules involved in microglial activation is galectin-3 (Gal-3). In recent years, extensive studies have dissected the mechanisms by which Gal-3 modulates microglial activation, impacting Aβ deposition, in both animal models and human studies. In this review article, we focus on the emerging role of Gal-3 in biology and pathobiology, including its origin, its functions in regulating microglial activation and neuroinflammation, and its emergence as a biomarker in AD and other neurodegenerative diseases. These aspects are important to elucidate the involvement of Gal-3 in AD pathogenesis and may provide novel insights into the use of Gal-3 for AD diagnosis and therapy.

Indexed as

Alzheimer’s diseaseAmyloid-βGalectin-3MicrogliaNeuroinflammation

Identifiers

PMID33906678
PMCPMC8077955
OpenAlexW3159005222

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.