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Blocking TSP1 Ameliorates Diabetes Mellitus-Induced Erectile Dysfunction by Inhibiting the TGF-β/SMAD Pathway.

Mancheng Xia1,2,3,4, Yiming Yuan1,2,3,4, Dong Fang1,2,3,4

  • 1Department of Urology, Peking University First Hospital, Beijing, China.

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|September 30, 2024
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Thrombospondin-1 (TSP1) drives fibrosis in diabetes mellitus-induced erectile dysfunction (DMED). The TSP1 antagonist LSKL improves erectile function by blocking the TGF-β/SMAD pathway, offering a potential therapeutic target.

Keywords:
Diabetes mellitusErectile dysfunctionFibrosisTransforming growth factor beta1

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Area of Science:

  • Urology
  • Endocrinology
  • Cell Biology

Background:

  • Diabetes mellitus-induced erectile dysfunction (DMED) is a complex condition often involving penile fibrosis.
  • The precise molecular mechanisms underlying fibrosis in DMED require further elucidation.
  • Thrombospondin-1 (TSP1) has been implicated in fibrotic processes, but its role in DMED is not fully understood.

Purpose of the Study:

  • To investigate the role and mechanism of TSP1 in the development of fibrosis in DMED.
  • To assess the therapeutic potential of LSKL, a TSP1 antagonist, in mitigating DMED-related fibrosis.

Main Methods:

  • DMED was induced in rats using streptozotocin; treatment groups included control, DMED, and DMED with LSKL administration.
  • Penile fibrosis was evaluated using Sirius red and Masson trichrome staining.
  • In vitro studies utilized high glucose-induced corpus cavernosum smooth muscle cells (CCSMCs) and fibroblasts (CCFs) treated with or without LSKL to assess TSP1 expression, TGF-β pathway activation, and collagen deposition via Western blotting and immunofluorescence.

Main Results:

  • DMED rats exhibited decreased intracavernous pressure (ICP)/mean arterial pressure (MAP) ratios and altered smooth muscle to collagen ratios, indicative of fibrosis.
  • TSP1 expression was significantly elevated in the corpus cavernosum (CC) of DMED rats and in HG-treated CCSMCs and CCFs.
  • LSKL treatment improved ICP/MAP ratios and collagen profiles in DMED rats and inhibited HG-induced TGF-β/SMAD pathway activation and collagen IV overexpression in CCSMCs.

Conclusions:

  • Elevated TSP1 expression in the CC contributes to penile fibrosis in DMED, potentially through autocrine and paracrine signaling.
  • High glucose conditions activate TSP1 secretion, promoting fibrosis via the TGF-β/SMAD pathway.
  • LSKL demonstrates therapeutic potential for DMED by antagonizing TSP1 and inhibiting the TGF-β/SMAD signaling pathway.