Evidence map›Paper›PMID 38693121›Full record

ArticleNature communications2024

Galectin-3 impairs calcium transients and β-cell function.

Qian Jiang, Qijin Zhao, Yibing Chen, Chunxiao Ma, Xiaohong Peng, Xi Wu, Xingfeng Liu, Ruoran Wang, Shaocong Hou, Lijuan Kong and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
5.8field-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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. PerturbingCells · 2026
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  13. 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
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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

16 authors at 4 institutions in 2 countries.

Qian Jiang *State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China.
Qijin Zhao *State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China.ORCID http://orcid.org/0000-0002-1216-1640
Yibing Chen *State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China.
Chunxiao Ma *State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China.
Xiaohong PengCollege of Future Technology, Institute of Molecular Medicine, National Biomedical Imaging Center, Peking University, Beijing, 100871, China.
Xi WuState Key Laboratory of Membrane Biology, College of Future Technology, Institute of Molecular Medicine, Peking University, Beijing, 100871, China.
Xingfeng LiuState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China.ORCID http://orcid.org/0000-0002-7518-5797
Ruoran WangSchool of Basic Medical Sciences, Zhejiang University, Hangzhou, Zhejiang, China.
Shaocong HouState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China.ORCID http://orcid.org/0000-0003-0442-8138
Lijuan KongState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China.ORCID http://orcid.org/0009-0005-7194-1443
Yanjun WanState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China.
Shusen WangOrgan Transplant Center, Tianjin First Central Hospital, Nankai University, Tianjin, 300192, China.ORCID http://orcid.org/0000-0002-2323-6564
Zhuo-Xian MengSchool of Basic Medical Sciences, Zhejiang University, Hangzhou, Zhejiang, China.ORCID http://orcid.org/0000-0001-8177-5593
Bing CuiState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China.ORCID http://orcid.org/0000-0001-8374-7801
Liangyi ChenCollege of Future Technology, Institute of Molecular Medicine, National Biomedical Imaging Center, Peking University, Beijing, 100871, China.ORCID http://orcid.org/0000-0003-1270-7321
Pingping LiState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China. lipp@imm.ac.cn.ORCID http://orcid.org/0000-0003-0679-270X
Chinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University · CNZhejiang University · CNNankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In diabetes, macrophages and inflammation are increased in the islets, along with β-cell dysfunction. Here, we demonstrate that galectin-3 (Gal3), mainly produced and secreted by macrophages, is elevated in islets from both high-fat diet (HFD)-fed and diabetic db/db mice. Gal3 acutely reduces glucose-stimulated insulin secretion (GSIS) in β-cell lines and primary islets in mice and humans. Importantly, Gal3 binds to calcium voltage-gated channel auxiliary subunit gamma 1 (CACNG1) and inhibits calcium influx via the cytomembrane and subsequent GSIS. β-Cell CACNG1 deficiency phenocopies Gal3 treatment. Inhibition of Gal3 through either genetic or pharmacologic loss of function improves GSIS and glucose homeostasis in both HFD-fed and db/db mice. All animal findings are applicable to male mice. Here we show a role of Gal3 in pancreatic β-cell dysfunction, and Gal3 could be a therapeutic target for the treatment of type 2 diabetes.

Indexed as

Diet, High-FatGalectin 3Insulin-Secreting CellsInsulin SecretionAnimalsBlood ProteinsCalciumCalcium ChannelsDiabetes Mellitus, Type 2GalectinsGlucoseHumansInsulinMacrophagesMaleMiceBlood ProteinsCalciumCalcium ChannelsGalectin 3GalectinsGlucoseInsulinLGALS3 protein, humanLgals3 protein, mouse

Identifiers

PMID38693121
PMCPMC11063191
OpenAlexW4396546319

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.