Feng Yin, Hongming Chen, Hongtai Tu, Hao Zhong, Yunqi Mo, Tianxiang Xie, Zhubinyun Lai, Junrong Zou, Rihai Xiao
This framework aligns model selection with clinical subtypes, improving translational mechanistic consistency. Future work should develop comorbid composite models and integrate clinical multi-omics stratification to enhance study design and therapeutic development.
BACKGROUND AND OBJECTIVE: Erectile dysfunction (ED) is a multifactorial condition with diverse underlying etiologies, including neurogenic, metabolic, vascular, hormonal, and psychogenic factors. Traditional animal models are often classified by induction technique (e.g., surgical, chemical) rather than by pathophysiological driver, limiting their translational relevance to specific clinical subtypes. This review proposes an etiology-oriented framework for rodent ED models, aiming to categorize models according to clinical causes and to summarize modeling strategies, key molecular mechanisms, and functional assessment methods for each category.
METHODS: We conducted a narrative review of PubMed, Web of Science, and Scopus (from database inception to December 2025) for English peer‑reviewed studies, supplemented by manual reference screening.
KEY CONTENT AND FINDINGS: Rodent ED models are grouped into neurogenic, metabolic/vascular, hormone-associated, and psychogenic categories. Common molecular endpoints include imbalance among the NO-cGMP-PKG relaxation axis, cAMP-PKA synergy, and RhoA/ROCK contraction. Principles for selecting intracavernous pressure (ICP)/mean arterial pressure (MAP), histological, and behavioral assessments are summarized.
CONCLUSIONS: This framework aligns model selection with clinical subtypes, improving translational mechanistic consistency. Future work should develop comorbid composite models and integrate clinical multi-omics stratification to enhance study design and therapeutic development.