Evidence map›Paper›PMID 38378809›Full record

ArticleCell death discovery2024

Galectin-3 is involved in inflammation and fibrosis in arteriogenic erectile dysfunction via the TLR4/MyD88/NF-κB pathway.

Guanbo Wang, Ruiyu Li, Chen Feng, Kefan Li, Shuai Liu, Qiang Fu

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
9.6field-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

22 citing papers in PubMed, 25 citations in OpenAlex.

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  18. Chimerolectins: Classification, structural architecture, and functional perspectives.Protein science : a publication of the Protein Society · 2025
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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

6 authors at 2 institutions in 1 country.

Guanbo WangDepartment of Urology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Ruiyu LiDepartment of Urology, Shandong Provincial Hospital, Shandong University, Jinan, China.
Chen FengDepartment of Urology, Shandong Provincial Hospital, Shandong University, Jinan, China.
Kefan LiDepartment of Urology, Shandong Provincial Hospital, Shandong University, Jinan, China.
Shuai LiuDepartment of Urology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China. liushuai@sdfmu.edu.cn.ORCID http://orcid.org/0000-0002-6259-2350
Qiang FuDepartment of Urology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China. qiangfu68@163.com.ORCID http://orcid.org/0000-0003-1916-1229
Shandong University · CNShandong Provincial Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82071635
6 · The paper itself

Abstract

Galectin-3 (Gal-3) is a multifunctional protein that has been linked to fibrosis and inflammation in the cardiovascular system. In this study, we examined the impact of Gal-3 on inflammation and fibrosis in patients with arteriogenic erectile dysfunction (A-ED) and the underlying mechanisms involved. To induce arterial injury, we utilized cuffs on the periaqueductal common iliac arteries of Sprague‒Dawley (SD) rats and administered a high-fat diet to co-induce local atherosclerosis. Our results showed that we successfully developed a novel A-ED model that was validated based on histological evidence. In vivo, the vascular lumen of rats subjected to a high-fat diet and cuff placement exhibited significant narrowing, accompanied by the upregulation of Gal-3, Toll-like receptor 4 (TLR4), and myeloid differentiation primary response protein 88 (MyD88) expression in the penile cavernosa. This led to the activation of nuclear factor kappa B 65 (NF-κB-p65), resulting in reduced intracavernosal pressure, endothelial nitric oxide synthase expression, and smooth muscle content, promoting inflammation and fibrosis. However, treatment with Gal-3 inhibitor-modified citrus pectin (MCP) significantly normalized those effects. In vitro, knocking down Gal-3 led to a significant reduction in TLR4, MyD88, and NF-κB-p65 expression in corpus cavernosum smooth muscle cells (CCSMCs), decreasing inflammation levels. In conclusion, inhibiting Gal-3 may improve A-ED by reducing inflammation, endothelial injury, and fibrosis in the penile corpus cavernosum through the TLR4/MyD88/NF-κB pathway. These findings highlight the potential therapeutic target of Gal-3 in A-ED.

Identifiers

PMID38378809
PMCPMC10879531
OpenAlexW4391955651

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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.