The association between TNF-α and erectile dysfunction complaints

Matos, Gabriela; Hirotsu, Camila; Alvarenga, Tathiana A.; Cintra, Fátima Dumas; Bittencourt, Lia; Tufik, Sérgio; Andersen, Mônica Levy

doi:10.1111/j.2047-2927.2013.00136.x

Cited by 37 publications

(32 citation statements)

References 41 publications

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“…Blood levels of TNFa, along with other pro-inflammatory (IL-6, IL-1b) and prothrombotic factors, were significantly increased in ED patients and negatively related to sexual performance (Vlachopoulos et al, 2006). Similar results were also found in patients with type 2 diabetes mellitus (Araña Rosaínz Mde et al, 2011) and in patients with obstructive sleep apnea syndrome (Matos et al, 2013). Animal models involving genetic manipulation of TNFa, have shown peculiar alterations of erectile function.…”

Section: Discussionsupporting

confidence: 56%

Nonalcoholic steatohepatitis as a novel player in metabolic syndrome-induced erectile dysfunction: An experimental study in the rabbit

Vignozzi

Filippi

Comeglio

et al. 2014

Molecular and Cellular Endocrinology

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a b s t r a c tA pathogenic link between erectile dysfunction (ED) and metabolic syndrome (MetS) is now well established. Nonalcoholic steatohepatitis (NASH), the hepatic hallmark of MetS, is regarded as an active player in the pathogenesis of MetS-associated cardiovascular disease (CVD). This study was aimed at evaluating the relationship between MetS-induced NASH and penile dysfunction. We used a non-genomic, high fat diet (HFD)-induced, rabbit model of MetS, and treated HFD rabbits with testosterone (T), with the selective farnesoid X receptor (FXR) agonist obeticholic acid (OCA), or with the anti-TNFa mAb infliximab. Rabbits fed a regular diet were used as controls. Liver histomorphological and gene expression analysis demonstrated NASH in HFD rabbits. Several genes related to inflammation (including TNFa), activation of stellate cells, fibrosis, and lipid metabolism parameters were negatively associated to maximal acetylcholine (Ach)-induced relaxation in penis. When all these putative liver determinants of penile Ach responsiveness were tested as covariates in a multivariate model, only the association between hepatic TNFa expression and Ach response was confirmed. Accordingly, circulating levels of TNFa were increased 15-fold in HFD rabbits. T and OCA dosing in HFD rabbits both reduced TNFa liver expression and plasma levels, with a parallel increase of penile eNOS expression and responsiveness to Ach. Also neutralization of TNFa with infliximab treatment fully normalized HFD-induced hypo-responsiveness to Ach, as well as responsiveness to vardenafil, a phosphodiesterase type 5 inhibitor. Thus, MetS-induced NASH in HFD rabhttp://dx

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Section: Discussionsupporting

confidence: 56%

Nonalcoholic steatohepatitis as a novel player in metabolic syndrome-induced erectile dysfunction: An experimental study in the rabbit

Vignozzi

Filippi

Comeglio

et al. 2014

Molecular and Cellular Endocrinology

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“…Moreover, other investigators reported that ED was associated with increased levels of TNF-a and CRP, which increased progressively with the severity of penile vascular disease, supporting the role of these markers in the pathophysiology of ED [22, 23]. Furthermore, recently, Matos et al showed that there was an association between TNF-a levels and ED complaints in men independent of OSAHS [24]. It is worth noting that, in a recent study, reduced levels of adiponectin, an anti-inflammatory cytokine that attenuates endothelial cell adhesion molecules, and the levels of inflammatory cytokines, such as TNF-a, IL-8, and IL-6, were observed in patients with ED [25].…”

Section: Discussionmentioning

confidence: 90%

Abnormal Cytokine Profile in Patients with Obstructive Sleep Apnea-Hypopnea Syndrome and Erectile Dysfunction

Bouloukaki

Papadimitriou

Sofras

et al. 2014

Mediators of Inflammation

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Patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) show a high prevalence of erectile dysfunction (ED). Although the underlying pathogenesis is still unknown, endothelial dysfunction, induced by inflammatory cytokines, chemokines, and adhesion molecules, has been proposed as a possible mechanism. The aim of this study was to assess whether OSAHS is associated with activation of the inflammatory cytokine system in patients with ED compared to the matched OSAHS patients with normal sexual function. Thirty-one patients with severe OSAHS and ED were included. Fifteen patients with severe OSAHS and without ED served as controls. Serum concentrations of high-sensitivity C-reactive protein (hsCRP), tumor necrosis factor-α (TNF-a), interleukin-6 (IL-6), interleukin-8 (IL-8), and adiponectin were measured after the diagnostic polysomnography. We found that hsCRP levels were significantly elevated in OSAHS patients with ED compared to controls. Similarly, TNF-a levels, IL-6, and IL-8 were elevated in OSAHS patients with ED compared to controls. Serum adiponectin levels were lower in OSAHS-ED patients, but the difference did not reach statistical significance. The presence of ED in patients with severe OSAHS is associated with elevated levels of inflammatory markers, underlining a possible involvement of endothelial dysfunction in the pathogenesis of ED.

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“…TNF‐α contributes to the dysregulation of insulin modulation of endothelin‐1‐mediated vasoconstriction and NO‐mediated vasodilation. It is likely that TNF‐α may reduce NO release and its metabolites, which, in turn, affects penile erection [101]. It has been suggested that increased expression of TNF‐α in obesity and subsequent reduced expression of adiponectin plays a significant role in development of the MetS [102].…”

Section: Inflammationmentioning

confidence: 99%

A Comprehensive Review of Metabolic Syndrome Affecting Erectile Dysfunction

Kaya

Sikka

Gür

2015

The Journal of Sexual Medicine

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Introduction Metabolic syndrome (MetS) is the most important public health issue threatening the health of men and women all over the world. Its current prevalence (i.e., approximately 30%) is continuously increasing. MetS by itself is considered a risk factor for erectile dysfunction (ED). Aim To focus on the definition epidemiology, pathogenesis, and possible mechanistic links between MetS and ED in order to provide guidelines for treating such individuals. Methods The search strategies yielded total records screened from PubMed. Main Outcome Measures Regardless of the definition, MetS consists of insulin resistance, hypertension, dyslipidemia, and obesity. MetS is not an end disease but is a disorder of energy utilization and storage. Results The prevalence of ED in patients with MetS is almost twice than in those without MetS, and about 40% of patients with ED have MetS. An important mechanism linking MetS and ED is hypogonadism. Conclusions Recognizing through ED, underlying conditions such as hypogonadism, diabetes and MetS might be a useful motivation for men to improve their health-related choices. The clinical management of MetS can be done by therapeutic interventions that include lifestyle modifications, hormone replacement alone or in combination with phosphodiesterase 5 inhibitors, and other pharmacological treatments.

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The association between TNF-α and erectile dysfunction complaints

Cited by 37 publications

References 41 publications

Nonalcoholic steatohepatitis as a novel player in metabolic syndrome-induced erectile dysfunction: An experimental study in the rabbit

Nonalcoholic steatohepatitis as a novel player in metabolic syndrome-induced erectile dysfunction: An experimental study in the rabbit

Abnormal Cytokine Profile in Patients with Obstructive Sleep Apnea-Hypopnea Syndrome and Erectile Dysfunction

A Comprehensive Review of Metabolic Syndrome Affecting Erectile Dysfunction

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