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Galectin-3 is involved in inflammation and fibrosis in arteriogenic erectile dysfunction via the TLR4/MyD88/NF-κB pathway.
Wang, Guanbo; Li, Ruiyu; Feng, Chen; Li, Kefan; Liu, Shuai; Fu, Qiang.
Afiliação
  • Wang G; Department of Urology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
  • Li R; Department of Urology, Shandong Provincial Hospital, Shandong University, Jinan, China.
  • Feng C; Department of Urology, Shandong Provincial Hospital, Shandong University, Jinan, China.
  • Li K; Department of Urology, Shandong Provincial Hospital, Shandong University, Jinan, China.
  • Liu S; Department of Urology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China. liushuai@sdfmu.edu.cn.
  • Fu Q; Department of Urology, Shandong Provincial Hospital, Shandong University, Jinan, China. liushuai@sdfmu.edu.cn.
Cell Death Discov ; 10(1): 92, 2024 Feb 20.
Article em En | MEDLINE | ID: mdl-38378809
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.

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Cell Death Discov Ano de publicação: 2024 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Cell Death Discov Ano de publicação: 2024 Tipo de documento: Article País de afiliação: China