There is a Link Between Erectile Dysfunction and Heart Failure: It could be Inflammation

Autor(es)

Rodrigues, Fernanda Luciano ^[1] ; Fais, Rafael Sobrano ^[1] ; Tostes, Rita C. ^[1] ; Carneiro, Fernando S. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pharmacol, BR-14049900 Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: CURRENT DRUG TARGETS; v. 16, n. 5, p. 442-450, 2015.
• Citações Web of Science: 7

Resumo

The rates of erectile dysfunction (ED) in heart failure (HF) are extremely high. Limited capacity of patients with HF to exercise and coronary artery disease are considered to be the main causative mechanisms. Both HF and ED are associated with increased levels of proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8). The increased levels of proinflammatory cytokines in ED suggest that inflammatory markers act as important active agents in ED development. The innate immune system also reacts to danger signals released by damaged cells. Damage-associated molecular patterns (DAMPs) are molecules released as a result of tissue injury acting on immune activation during non-infectious inflammation. DAMPs may also reach the circulation and mediate pathophysiological processes that occur in distant organs to the injured site. Cardiomyocytes possess abundant mitochondria and during tissue damage, it is likely that the heart releases high amounts of mitochondrial DNA (mtDNA), which acts as a potent ligand for Toll-like receptor 9 (TLR9). Accordingly, in the present manuscript we review the literature pertaining the relationship between HF and ED and the subjacent inflammatory process associated to both diseases. In addition, we propose the hypothesis that TLR9 activation by DAMPs released in HF leads to inflammation, vascular dysfunction and functional changes in cavernosal tissue, providing an additional mechanism that connects HF to ED. Since TNF-alpha usually is a product of TLRs activation and seems to be a common link between HF and ED, our hypothesis provide two possible targets to treat the ED associated to HF and may have important preventative and therapeutic implications. (AU)

• Processo FAPESP: 10/17362-4 - Mecanismos da disfunção erétil na insuficiência cardíaca
• Beneficiário: Fernando Silva Carneiro
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores