Background:
Erectile dysfunction (ED) is an evolving health problem in the aging male population.
Chronic low-grade inflammation is a critical component of ED pathogenesis and a probable intermediate stage of
endothelial dysfunction, especially in metabolic diseases, with the inclusion of obesity, metabolic syndrome, and
diabetes.
Objective:
This review will present an overview of preclinical and clinical data regarding common inflammatory
mechanisms involved in the pathogenesis of ED associated with metabolic diseases and the effect of antiinflammatory
drugs on ED.
Methods:
A literature search of existing pre-clinical and clinical studies was performed on databases [Pubmed
(MEDLINE), Scopus, and Embase] from January 2000 to October 2019.
Results:
Low-grade inflammation is a possible pathological role in endothelial dysfunction as a consequence of
ED and other related metabolic diseases. Increased inflammation and endothelial/prothrombotic markers can be
associated with the presence and degree of ED. Pharmacological therapy and modification of lifestyle and risk
factors may have a significant role in the recovery of erectile response through reduction of inflammatory marker
levels.
Conclusion:
Inflammation is the least common denominator in the pathology of ED and metabolic disorders. The
inflammatory process of ED includes a shift in the complex interactions of cytokines, chemokines, and adhesion
molecules. These data have established that anti-inflammatory agents could be used as a therapeutic opportunity
in the prevention and treatment of ED. Further research on inflammation-related mechanisms underlying ED and
the effect of therapeutic strategies aimed at reducing inflammation is required for a better understanding of the
pathogenesis and successful management of ED.
Early features of systemic and adipose-tissue low-grade inflammation in a
model of postprandial endothelial dysfunction