ArticleStem cells international2026
Intracavernous Injection of Mechanically Extracted Stromal Vascular Fragments Suppresses Endothelial-Mesenchymal Transformation to Mitigate Erectile Dysfunction in Hypertensive Rats.
Article in Stem cells international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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1 citing paper in PubMed.
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Erectile dysfunction (ED) is widespread among individuals with high blood pressure and negatively affects quality of life. The effect of stromal vascular fraction (SVF) on hypertension-related ED remains unexplored. We used a hypertensive rat model to explore the relative efficacy of adipose tissue stromal vascular fraction (tSVF) and cellular SVF (cSVF). We then investigated the possible mechanisms of these treatments. Hypertensive rats were divided into three groups according to different treatments. Their intracavernous pressure (ICP) during erection and condition of cavernous tissue were compared to those of the controlled group. Endothelial-mesenchymal transformation (EndMT) markers as well as related inflammatory factors were also measured. cSVF and tSVF were labeled with CM-Dil before injection in order to determine whether cSVF and tSVF survived, proliferated, and transdifferentiated in vivo. The increased ICP during erection demonstrated that tSVF treatment significantly improved hypertension-related ED. tSVF increased the smooth muscle-to-collagen ratio and inhibiting the expression of fibrosis-related proteins in hypertensive rats while rescuing the expression of vWF and eNOS, which indicated the preserving of endothelial tissue of the penis. Immunofluorescence staining and western blotting of penile tissue clearly suggest the inhibitory effect of tSVF on the overoccurring EndMT. Immunofluorescence staining and Western blot analysis of endothelial cells in vitro corroborate the whole-tissue findings. The experiments in N-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced human umbilical vein endothelial cells (HUVECs) revealed tSVF suppresses EndMT via inhibiting the TGF-
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