Vascular endothelium is the basic way for stem cells to treat erectile dysfunction: a bibliometric study

Abstract

Vascular endothelial is considered to be a key factor in the pathogenesis of erectile dysfunction (ED). The purpose is to reveal the research trend of the field of ED and vascular endothelium. In addition, the goal is to discover the role and mechanism of vascular endothelium in ED. Bibliometrics and visualization methods based on CiteSpace were selected. We conducted the co-authorship analysis of countries, institutions and authors, co-occurrence analysis of keywords, and co-citation analysis of literature and authors through CiteSpace 6.1.R3. 1431 articles from Web of Science Core Collection (WOSCC) were included in the analysis from 1991 to 2022. We found some influential and cutting-edge nodes in each map, including countries, institutions, authors, articles, etc. Stem cell, therapy, oxidative stress, cavernous nerve injury, radical prostatectomy, fibrosis, erectile function, mesenchymal stem cell, and apoptosis may be hot keywords. In conclusion, the efficacy and mechanisms of stem cells and their derivatives in the treatment of diabetes (DM) ED and cavernous nerve injury (CNI) ED are the future research trends. Stem cells therapy for ED is a hot spot in this field, which side notes that stem cells may work mainly through improving endothelial function. Vascular endothelial cells and VEGF may repair nerve and cavernous smooth muscle directly or indirectly, and finally polish up erectile function.

Exosomes derived from mesenchymal stem cells in diabetes and diabetic complications

“…More than half of men with DM have erectile dysfunction (ED) worldwide, with a prevalence 3.5‐fold times higher than those without DM [ 159 ]. Diabetic erectile dysfunction (DED) involves multiple pathogenesis, such as the dysregulation of VEGF signaling transduction due to hyperglycemia, elevated levels of advanced glycation end products (AGEs), the synthesis of nitric oxide synthase (NOS), heightened production of oxygen free radicals in neurons, and reduced NO and cyclic guanosine monophosphate (cGMP)-dependent protein kinase-1 (cGKI) [ 160 ]. The deleterious effects of hyperglycemia and endothelial dysfunction of the vascular lining caused by oxidative stress is the basic pathophysiology of DED.…”