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Experimental models of Peyronie's disease. Implications for new therapies
Nestor F Gonzalez-Cadavid1, Jacob Rajfer
1Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center-Urology Research Laboratory, Torrance, CA, USA. ncadavid@ucla.edu
Introduction:
Despite its high prevalence and impact on the quality of life of patients, and that it is an excellent model for the study of fibrotic processes, Peyronie's disease (PD) is an orphan disease in biomedical research. The development of animal and cell culture models has advanced substantially the understanding of its molecular and cellular pathology and the proposal of new therapies.
Aim:
To review the literature pertaining to the use of these models for the study of PD.
Methods:
PubMed search conducted from the first report of an animal model for PD.
Results:
This model, based on the finding that transforming growth factor beta1 (TGF beta 1) is overexpressed in the PD plaque, consists on the injection of TGF beta 1 into the tunica albuginea of the rat. This leads to a PD-like plaque retaining many of the histological and biochemical features of human PD. Another rat model, based on the hypothesis that the PD plaque arises from trauma to the penis, causing fibrinogen extravasation that initiates as fibrin a fibrotic response, consists on injection of fibrin into the tunica. The cell culture model is based on the demonstration that myofibroblasts are abundant in the human PD plaque.
Conclusions:
These models have: (i) clarified the role of microtrauma, myofibroblasts, and oxidative stress in plaque development; (ii) demonstrated that this tissue is under sustained turnover by fibrotic and antifibrotic mechanisms; (iii) showed the interplay of collagenolytic and fibrinolytic systems and their inhibitors; (iv) detected an endogenous antifibrotic process consisting of the expression of inducible nitric oxide synthase that counteracts oxidative stress, collagen synthesis, and myofibroblast generation; (v) characterized the antifibrotic effects of chronic treatment with phosphodiesterase type 5 (PDE5) inhibitors; (vi) discovered the cytogenetic instability of PD cells and alterations in their gene expression; and (vii) detected stem cells in the tunica albuginea with a potential role in fibrosis and ossification.
Insights
Animal and cell models advance Peyronie's disease (PD) research. These models clarify plaque development, identify antifibrotic mechanisms, and reveal potential therapeutic targets for this fibrotic condition.
Area of Science:
- Urology
- Fibrotic Diseases
- Biomedical Research Models
Background:
- Peyronie's disease (PD) is a prevalent fibrotic condition impacting patient quality of life.
- Despite its significance, PD remains under-researched, classifying it as an orphan disease.
- Advancements in animal and cell models have improved understanding of PD's pathology and therapeutic strategies.
Purpose of the Study:
- To conduct a literature review on existing animal and cell culture models for studying Peyronie's disease.
- To summarize the utility of these models in advancing PD research.
Main Methods:
- Literature search of PubMed database for studies reporting animal models of PD.
- Analysis of established animal (rat-based TGF-β1 and fibrin injection) and cell culture models.
Main Results:
- TGF-β1 injection in rats creates a PD-like plaque with human PD features.
- Fibrin injection in rats models PD plaque development following trauma.
- Cell culture models utilize myofibroblasts, abundant in human PD plaques.
Conclusions:
- Models elucidated roles of microtrauma, myofibroblasts, and oxidative stress in PD.
- Demonstrated continuous fibrotic and antifibrotic tissue turnover in PD.
- Revealed interplay of collagenolytic/fibrinolytic systems and identified endogenous antifibrotic mechanisms (e.g., inducible nitric oxide synthase).
- Characterized antifibrotic effects of phosphodiesterase type 5 (PDE5) inhibitors.
- Discovered cytogenetic instability and gene expression alterations in PD cells.
- Identified stem cells in tunica albuginea with potential roles in fibrosis and ossification.
