Biljana Musicki1, Anthony J Bella2, Trinity J Bivalacqua1, Kelvin P Davies3, Michael E DiSanto4, Nestor F Gonzalez-Cadavid5,6, Johanna L Hannan7, Noel N Kim8, Carol A Podlasek9, Christopher J Wingard7, Arthur L Burnett1. 1. The James Buchanan Brady Urological Institute and Department of Urology, The Johns Hopkins School of Medicine, Baltimore, MD, USA. 2. Division of Urology, Department of Surgery and Department of Neuroscience, Ottawa Hospital Research Institute at the University of Ottawa, Ottawa, ON, Canada. 3. Department of Urology, Albert Einstein College of Medicine, New York, NY, USA. 4. Department of Surgery/Division of Urology, Cooper University Hospital, Camden, NJ, USA. 5. Division of Urology, Department of Surgery, Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, USA. 6. Department of Urology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA. 7. Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA. 8. Institute for Sexual Medicine, San Diego, CA, USA. 9. Departments of Urology, Physiology, and Bioengineering, University of Illinois at Chicago, Chicago, IL, USA.
Abstract
INTRODUCTION: Although clinical evidence supports an association between cardiovascular/metabolic diseases (CVMD) and erectile dysfunction (ED), scientific evidence for this link is incompletely elucidated. AIM: This study aims to provide scientific evidence for the link between CVMD and ED. METHODS: In this White Paper, the Basic Science Committee of the Sexual Medicine Society of North America assessed the current literature on basic scientific support for a mechanistic link between ED and CVMD, and deficiencies in this regard with a critical assessment of current preclinical models of disease. RESULTS: A link exists between ED and CVMD on several grounds: the endothelium (endothelium-derived nitric oxide and oxidative stress imbalance); smooth muscle (SM) (SM abundance and altered molecular regulation of SM contractility); autonomic innervation (autonomic neuropathy and decreased neuronal-derived nitric oxide); hormones (impaired testosterone release and actions); and metabolics (hyperlipidemia, advanced glycation end product formation). CONCLUSION: Basic science evidence supports the link between ED and CVMD. The Committee also highlighted gaps in knowledge and provided recommendations for guiding further scientific study defining this risk relationship. This endeavor serves to develop novel strategic directions for therapeutic interventions.
INTRODUCTION: Although clinical evidence supports an association between cardiovascular/metabolic diseases (CVMD) and erectile dysfunction (ED), scientific evidence for this link is incompletely elucidated. AIM: This study aims to provide scientific evidence for the link between CVMD and ED. METHODS: In this White Paper, the Basic Science Committee of the Sexual Medicine Society of North America assessed the current literature on basic scientific support for a mechanistic link between ED and CVMD, and deficiencies in this regard with a critical assessment of current preclinical models of disease. RESULTS: A link exists between ED and CVMD on several grounds: the endothelium (endothelium-derived nitric oxide and oxidative stress imbalance); smooth muscle (SM) (SM abundance and altered molecular regulation of SM contractility); autonomic innervation (autonomic neuropathy and decreased neuronal-derived nitric oxide); hormones (impaired testosterone release and actions); and metabolics (hyperlipidemia, advanced glycation end product formation). CONCLUSION: Basic science evidence supports the link between ED and CVMD. The Committee also highlighted gaps in knowledge and provided recommendations for guiding further scientific study defining this risk relationship. This endeavor serves to develop novel strategic directions for therapeutic interventions.
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