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Published on: March 15, 2024
Mechanisms of penile fibrosis
1Los Angeles Biomedical Research Institute (LABioMed) at Harbor-UCLA Medical Center-Urology Research Laboratory, Division of Urology, Torrance, CA 90509, USA. ncadavid@ucla.edu
Introduction:
Penile fibrosis has been conceptually identified with the plaque that develops in the tunica albuginea in Peyronie's disease (PD), or with localized processes induced in the corpora cavernosa by ischemic or traumatic events. Recently, it has been proposed that a diffuse, progressive, and milder intracorporal fibrosis, which affects also the media of the penile arteries, is responsible for vasculogenic erectile dysfunction (ED) associated with aging, smoking, diabetes, hypertension, and post-radical prostatectomy. These processes differ in etiology, time course, target cells, and treatment, but have many features in common.
Aim:
To review the literature pertaining to fibrosis in the penis, related to PD and ED.
Methods:
PubMed search for pertinent publications mainly during 2001-2008.
Results:
This review focuses initially on PD and then deals with studies on ED in animal and cell culture models, discussing some of the pathophysiological similarities between tunical fibrosis in PD and corporal fibrosis in corporal veno-occlusive dysfunction (CVOD), and emerging therapeutic strategies. The role of profibrotic factors, the excessive deposit of collagen fibers and other extracellular matrix, the appearance of a synthetic cell phenotype in smooth muscle cells or the onset of a fibroblast-myofibroblast transition, and in the case of the corporal or penile arterial tissue the reduction of the smooth muscle cellular compartment, are discussed. This histopathology leads either to localized plaques or nodules in penile tissues, or to the diffuse fibrosis causing impairment of tissue compliance that underlies CVOD and arteriogenic ED. The antifibrotic role of the sustained stimulation of the nitric oxide/cyclic guanosine monophosphate pathway in the penis and its possible relevance to exogenous and endogenous stem cell differentiation is also briefly presented.
Conclusions:
Fibrotic processes in penile tissues share a similar cellular and molecular pathophysiology and common endogenous mechanisms of defense that have inspired novel pharmacological experimental approaches.
Insights
Penile fibrosis, linked to Peyronie's disease (PD) and erectile dysfunction (ED), involves similar cellular processes. Research highlights shared pathophysiology and defense mechanisms for novel therapeutic strategies.
Area of Science:
- Urology
- Andrology
- Cellular and Molecular Biology
Background:
- Penile fibrosis manifests as Peyronie's disease (PD) plaques or corporal fibrosis in erectile dysfunction (ED).
- Diffuse fibrosis affects penile arteries, contributing to ED in aging, diabetes, and post-surgery.
- These conditions share common underlying cellular and molecular mechanisms despite differing causes.
Purpose of the Study:
- To review existing literature on penile fibrosis in relation to PD and ED.
- To explore the pathophysiological similarities and differences between fibrotic processes in PD and ED.
- To discuss emerging therapeutic strategies for penile fibrosis.
Main Methods:
- Literature review of PubMed publications primarily from 2001-2008.
- Analysis of studies on PD and ED, including animal and cell culture models.
- Focus on cellular and molecular aspects of fibrosis and potential treatments.
Main Results:
- Penile fibrosis involves excessive collagen deposition, smooth muscle cell changes, and reduced cellularity.
- Histopathology results in localized plaques (PD) or diffuse fibrosis impairing tissue compliance (ED).
- The nitric oxide pathway and stem cell differentiation show potential antifibrotic roles.
Conclusions:
- Penile fibrotic processes share common cellular and molecular pathophysiology.
- Endogenous defense mechanisms against fibrosis offer insights for new treatments.
- Novel pharmacological approaches are inspired by these shared mechanisms.
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