Pyroptosis and inflammation-mediated endothelial dysfunction may act as key factors in the development of erectile dysfunction (Review)

Erectile dysfunction (ED) is a prevalent disease that causes sexual dysfunction in males. Inflammation-induced endothelial dysfunction is a fundamental pathophysiological symptom of ED, which is impacted by cell death. Pyroptosis is a type of programmed cell death mediated by the inflammasome that was discovered in inflammatory disorders. The activation of nucleotide-binding oligomerization domain-like receptors, particularly downstream inflammatory factors, such as IL-1 & beta; and IL-18, is indicative of caspase-dependent pyroptosis. Although the underlying mechanisms of pyroptosis have been investigated in several disorders, the role of pyroptosis in ED remains to be fully elucidated. At present, studies on pyroptosis have focused on improving the understanding of ED pathogenesis and promoting the development of novel therapeutic options. The present review article aimed to discuss the literature surrounding the mechanisms underlying pyroptosis, and summarize the role of pyroptosis in the development and progression of inflammation-mediated ED.

Automated summary

Erectile dysfunction (ED) is a common disease that results in sexual dysfunction in men. Inflammation-induced endothelial dysfunction, influenced by cell death, plays a critical role in the pathophysiology of ED. Pyroptosis, a type of programmed cell death mediated by the inflammasome, has been discovered in inflammatory disorders. However, the role of pyroptosis in ED is not fully understood. Research on pyroptosis aims to enhance the understanding of ED pathogenesis and develop new therapeutic options. This review discusses the literature on pyroptosis mechanisms and summarizes its role in the development and progression of inflammation-mediated ED.