madman
Super Moderator
Abstract
Erectile dysfunction (ED), which is defined as the inability to attain and maintain a satisfactory penile erection to sufficiently permit sexual intercourse, is a consequence and also a cause of cardiometabolic disorders like diabetes mellitus, systemic hypertension, central obesity, and dyslipidemia. Although there are mounting and convincing pieces of evidence in the literature linking ED and cardiometabolic disorders, impairment of nitric oxide-dependent vasodilatation seems to be the primary signaling pathway. Studies have also implicated the suppression of circulating testosterone, increased endothelin-1,and hyperactivation of Ang II/ATIr in the pathogenesis of ED and cardiometabolic disorders. This study provides comprehensive details of the association between cardiometabolic disorders and ED and highlights the mechanisms involved. This would open areas to be explored as therapeutic targets in the management of ED and cardiometabolic disorders. It also provides sufficient evidence establishing the need for the management of cardiometabolic disorders as an adjunct therapy in the management of ED.
Cardiometabolic Disorders
Cardiometabolic disorder is a group of metabolic risk factors for atherosclerosis such as insulin resistance or diabetes mellitus, systemic hypertension, central obesity, and dyslipidemia [9]. These predisposing factors contribute significantly to the global mortality and morbidity rate and hence remain a public health issue. Cardiometabolic disorder may be a consequence or cause of ED. Studies have established the role of arterial thickening and atherosclerosis, vascular endothelial damage, and remodeling in the pathogenesis of cardiometabolic disorder [10, 11]. The roles of antioxidants and oxidative stress in endothelial injury and cardiometabolic disorder have also been documented [9, 12]. These factors are also essential in the aetiopathogenesis of ED.
Erectile (dys)function: Physiology and Pathophysiology
*Physiology of Erection
*Pathophysiology of ED
*Obesity and ED
*Diabetes and ED
*Hypertension and ED
*ED as a Harbinger of Cardiometabolic Disorders
Nitric Oxide: A Key Player in the Pathogenesis of ED and Cardiometabolic Disorders
Testosterone: For Optimal Erectile Function or Cardiometabolic Function?
Taken together, testosterone is a common factor in the development of ED and cardiometabolic diseases. It is required for the physiological release of neurotransmitters in male sexual function and regulates the structure and function of penile vessels. In cardiometabolic function, testosterone ensures the normal structure of the arterial wall, inhibits the mediators of the inflammatory response (TNF alpha) and C-reactive protein, and also prevents vascular stiffening and calcification even though testosterone supplementation may increase cardiovascular risk.
Conclusion and Future Perspectives
Available evidence in the literature revealed that ED may be a cause and/or consequence of cardiometabolic disorders, which are risk factors for cardiovascular diseases. There are compelling pieces of evidence linking ED and cardiometabolic disorders; nonetheless, impairment of nitric oxide-dependent vasodilatation is the primary signaling pathway. Suppression of circulating testosterone increased endothelin-1, and hyperactivation of Ang II/ATIr are also essential key players in the pathogenesis of ED and cardiometabolic disorders. Although there are available strategies employed in the management of cardiometabolic disorders that are useful in preventing incident ED, this study provides a detailed update on the links between cardiometabolic disorders and ED, thus opening a window of opportunities to be explored for potential therapeutic targets in the management of ED and cardiometabolic disorder.
Erectile dysfunction (ED), which is defined as the inability to attain and maintain a satisfactory penile erection to sufficiently permit sexual intercourse, is a consequence and also a cause of cardiometabolic disorders like diabetes mellitus, systemic hypertension, central obesity, and dyslipidemia. Although there are mounting and convincing pieces of evidence in the literature linking ED and cardiometabolic disorders, impairment of nitric oxide-dependent vasodilatation seems to be the primary signaling pathway. Studies have also implicated the suppression of circulating testosterone, increased endothelin-1,and hyperactivation of Ang II/ATIr in the pathogenesis of ED and cardiometabolic disorders. This study provides comprehensive details of the association between cardiometabolic disorders and ED and highlights the mechanisms involved. This would open areas to be explored as therapeutic targets in the management of ED and cardiometabolic disorders. It also provides sufficient evidence establishing the need for the management of cardiometabolic disorders as an adjunct therapy in the management of ED.
Cardiometabolic Disorders
Cardiometabolic disorder is a group of metabolic risk factors for atherosclerosis such as insulin resistance or diabetes mellitus, systemic hypertension, central obesity, and dyslipidemia [9]. These predisposing factors contribute significantly to the global mortality and morbidity rate and hence remain a public health issue. Cardiometabolic disorder may be a consequence or cause of ED. Studies have established the role of arterial thickening and atherosclerosis, vascular endothelial damage, and remodeling in the pathogenesis of cardiometabolic disorder [10, 11]. The roles of antioxidants and oxidative stress in endothelial injury and cardiometabolic disorder have also been documented [9, 12]. These factors are also essential in the aetiopathogenesis of ED.
Erectile (dys)function: Physiology and Pathophysiology
*Physiology of Erection
*Pathophysiology of ED
*Obesity and ED
*Diabetes and ED
*Hypertension and ED
*ED as a Harbinger of Cardiometabolic Disorders
Nitric Oxide: A Key Player in the Pathogenesis of ED and Cardiometabolic Disorders
Testosterone: For Optimal Erectile Function or Cardiometabolic Function?
Taken together, testosterone is a common factor in the development of ED and cardiometabolic diseases. It is required for the physiological release of neurotransmitters in male sexual function and regulates the structure and function of penile vessels. In cardiometabolic function, testosterone ensures the normal structure of the arterial wall, inhibits the mediators of the inflammatory response (TNF alpha) and C-reactive protein, and also prevents vascular stiffening and calcification even though testosterone supplementation may increase cardiovascular risk.
Conclusion and Future Perspectives
Available evidence in the literature revealed that ED may be a cause and/or consequence of cardiometabolic disorders, which are risk factors for cardiovascular diseases. There are compelling pieces of evidence linking ED and cardiometabolic disorders; nonetheless, impairment of nitric oxide-dependent vasodilatation is the primary signaling pathway. Suppression of circulating testosterone increased endothelin-1, and hyperactivation of Ang II/ATIr are also essential key players in the pathogenesis of ED and cardiometabolic disorders. Although there are available strategies employed in the management of cardiometabolic disorders that are useful in preventing incident ED, this study provides a detailed update on the links between cardiometabolic disorders and ED, thus opening a window of opportunities to be explored for potential therapeutic targets in the management of ED and cardiometabolic disorder.
