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Androgens and morphologic remodeling at penile and cardiovascular levels: a common piece in complicated puzzles?
Vincenzo Mirone1, Ciro Imbimbo, Ferdinando Fusco
1Department of Urology-University Federico II, Naples, Italy.
Insights
Normal androgen levels protect cardiovascular and erectile health by maintaining tissue structure. Low androgen levels contribute to tissue remodeling and dysfunction in both systems.
Area of Science:
- Endocrinology
- Cardiovascular Biology
- Urology
Background:
- Epidemiologic data indicate normal androgen levels protect cardiovascular health and erectile function.
- Low androgen levels are linked to erectile dysfunction and increased cardiovascular disease risk.
- Both conditions involve pathological structural remodeling in tissues.
Purpose of the Study:
- To review androgen-dependent molecular signaling pathways and cellular events in penile and cardiovascular tissues.
- To understand androgen's role in tissue homeostasis and remodeling under normal and low levels.
- To explore mechanisms of androgen action in male health.
Main Methods:
- Literature search of Medline database (November 2008).
- Included studies from 1998-2008 on androgen mechanisms in penile and cardiovascular remodeling.
- Used keywords: androgens, hypogonadism, vessel tissue architecture, remodeling, cardiovascular system, penis.
Main Results:
- Androgens have direct beneficial effects on cardiovascular and penile tissues.
- Endothelial and smooth muscle cells are key targets, involved in remodeling.
- Low androgens lead to cell apoptosis, impaired progenitor cell function, and tissue remodeling.
Conclusions:
- Normal androgens maintain vascular and penile homeostasis via endothelial and smooth muscle cells.
- Low androgens disrupt these mechanisms, causing pathological structural remodeling.
- Androgen deficiency impacts male cardiovascular and erectile health through cellular and tissue changes.
Context:
Epidemiologic data demonstrate a protective role by normal androgen levels on cardiovascular health and erectile function. Low androgen levels are associated with erectile dysfunction and increased risk of cardiovascular diseases. Both conditions recognize as anatomic substrate a pathologic structural remodeling. Direct androgen effects on male external genitalia, vascular wall, and myocardium have been reported.
Objective:
To review current knowledge about androgen-dependent molecular signaling pathways and cellular events within penile and cardiovascular tissues involved in the homeostatic control of morphologic tissue properties and in the development of structural remodeling in presence of normal and low androgen levels, respectively.
Evidence Acquisition:
A literature search was performed in November 2008 using the commercially available Medline online engine search to retrieve studies (from 1998 to 2008) on the mechanisms mediating the role of androgens on penile and cardiovascular morphologic homeostasis and remodeling. A combination of the following medical subject headings was used: androgens, hypogonadism, vessel tissue architecture, remodeling, cardiovascular system, and penis.
Evidence Synthesis:
Androgens exert direct beneficial effects on both cardiovascular and penile tissues. Endothelial cells and smooth-muscle cells are the main cellular targets for direct androgen effects in both tissues and are involved in pathologic remodeling in hypogonadal models. At vascular level, androgens promote endothelial cell survival, reduce endothelial expression of proinflammatory markers, and inhibit proliferation and intimal migration of vascular smooth-muscle cells. At penile level, low androgen levels are associated with apoptosis of endothelial cells and smooth-muscle cells. Moreover, low androgen levels impair proliferation, migration, and homing of endothelial progenitor cells as well as myogenic differentiation of mesenchymal progenitor cells.
Conclusions:
Normal androgen levels promote vascular and penile homeostasis by direct mechanisms mainly involving endothelial cells and smooth-muscle cells. Low androgen levels are associated with impairments of such mechanisms, leading to pathologic structural remodeling.
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