Evidence map›Paper›PMID 33158139›Full record

ArticleInternational journal of molecular sciences2020

Galectin-3 Modulates Macrophage Activation and Contributes Smooth Muscle Cells Apoptosis in Abdominal Aortic Aneurysm Pathogenesis.

Hsin-Ying Lu, Chun-Ming Shih, Chun-Yang Huang, Alexander T H Wu, Tsai-Mu Cheng, Fwu-Long Mi, Chun-Che Shih

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Hsin-Ying LuDivision of Cardiovascular Surgery, Department of Surgery, Wan Fang Hospital, Taipei Medical University, Taipei 116, Taiwan.
Chun-Ming ShihTaipei Heart Institute, Taipei Medical University, Taipei 110, Taiwan.
Chun-Yang HuangDivision of Cardiovascular Surgery, Department of Surgery, Taipei Veterans General Hospital, Taipei 112, Taiwan.
Alexander T H WuThe Ph.D. Program for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan.ORCID 0000-0002-0178-6530
Tsai-Mu ChengThe Ph.D. Program for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan.ORCID 0000-0002-5712-3920
Fwu-Long MiDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.
Chun-Che ShihDivision of Cardiovascular Surgery, Department of Surgery, Wan Fang Hospital, Taipei Medical University, Taipei 116, Taiwan.
National Yang Ming Chiao Tung University · TWTaipei Medical University · TW

Funding

Taipei Medical University TMU108-F-005Wan Fang Hospital, Taipei Medical University 109TMU-WFH-19Wan Fang Hospital, Taipei Medical University 109-wf-eva-02Wan Fang Hospital, Taipei Medical University 109-wf-eva-07
6 · The paper itself

Abstract

Galectin-3 (Gal-3) is a 26-kDa lectin that regulates many aspects of inflammatory cell behavior. We assessed the hypothesis that increased levels of Gal-3 contribute to abdominal aortic aneurysm (AAA) progression by enhancing monocyte chemoattraction through macrophage activation. We analyzed the plasma levels of Gal-3 in 76 patients with AAA (AAA group) and 97 controls (CTL group) as well as in angiotensin II (Ang-II)-infused ApoE knockout mice. Additionally, conditioned media (CM) were used to polarize THP-1 monocyte to M1 macrophages with or without Gal-3 inhibition through small interfering RNA targeted deletion to investigate whether Gal-3 inhibition could attenuate macrophage-induced inflammation and smooth muscle cell (SMC) apoptosis. Our results showed a markedly increased expression of Gal-3 in the plasma and aorta in the AAA patients and experimental mice compared with the CTL group. An in vitro study demonstrated that the M1 cells exhibited increased Gal-3 expression. Gal-3 inhibition markedly decreased the quantity of macrophage-induced inflammatory regulators, including IL-8, TNF-α, and IL-1β, as well as messenger RNA expression and MMP-9 activity. Moreover, Gal-3-deficient CM weakened SMC apoptosis through Fas activation. These findings prove that Gal-3 may contribute to AAA progression by the activation of inflammatory macrophages, thereby promoting SMC apoptosis.

Indexed as

AgedAged, 80 and overAnimalsAorta, AbdominalAortic Aneurysm, AbdominalApoptosisBlood ProteinsCase-Control StudiesCells, CulturedFemaleGalectinsHumansMacrophage ActivationMacrophagesMaleMiceBlood ProteinsGalectinsLGALS3 protein, humanabdominal aortic aneurysmGalectin-3macrophage

Identifiers

PMID33158139
PMCPMC7663490
OpenAlexW3097711803

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Registered trials

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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.