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Author: Admin | 2025-04-28
Membrane released from the injured vessels and are considered a marker of endothelial dysfunction. Their concentration increases in patients with LOH and ED (54). Endothelial progenitor cells (EPCs) are a group of cells, similar to the embryonic angioblasts, that can originate from the mesoderm or from transdifferentiated monocyte/macrophages. EPCs could have different possible phenotypes and are implicated in the vasculogenic reparative process and the consequent re-endothelization after vascular injuries (54). Some EPC populations are decreased in hypogonadal patients (55), while other EPCs subtypes are present in higher concentration in patients with hypogonadism and ED, compared to eugonadal patients with ED (56). This last subpopulation of EPCs (i.e., EPCs CD45neg/CD34pos/CD144pos) could be considered a marker of vascular damage, in response to which they are produced in greater quantities in the attempt to repair the injured endothelium. In fact, they have been found in higher concentrations in the blood of patients with coronary artery disease, and their levels increase as ED worsens (54, 57). Furthermore, it has been shown that a greater endothelial damage is related to a worse pharmacological response to PDE5i (58).The oxidative stress is another mechanism by which hypogonadism affects endothelial function. In fact, it has been shown that hypogonadism increases oxidative stress and decreases NO bioavailability (59–61). Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is an enzymatic complex that catalyzes the production of reactive oxygen species (ROS) (62). In castrated rats some NADPH oxidase subunits are over-expressed and this up-regulation leads to increased ROS production in the corpora cavernosa
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