# Comprehensive proteomic characterization of urethral stricture disease in the Chinese population

## TL;DR

This study explores the proteomic profile of urethral stricture disease in Chinese patients, identifying key molecular pathways and potential treatments based on age groups.

## Contribution

The study provides new insights into the molecular mechanisms of scar formation in USD and identifies age-specific therapeutic strategies.

## Key findings

- Extracellular matrix and complement cascade signaling are prominent in scar tissues.
- COL11A1 and CD248 contribute to ECM accumulation in USD.
- Inhibiting the complement system may be a potential treatment for older USD patients.

## Abstract

Male urethral stricture disease (USD) is predominantly characterized by scar formation. There are few effective therapeutic drugs, and comprehensive molecular characterizations of USD formation remain undefined.

The proteomic profiling of twelve scar tissues and five matched normal adjacent tissues (NATs). Proteomic analysis methods were applied to explore the molecular characterizations of USD formation, including uncovering mechanistic pathways and providing novel biomarkers for scar formation.

Comparative proteomic analysis showed that the extracellular matrix (ECM) and complement cascade signaling were predominant in scar tissues. COL11A1 and CD248 significantly contributed to the accumulation of ECM components. Our study presented diverse molecular mechanisms of scar formation across different ages and suggested the potential effects of PXK in Age 1 (<45) patients. Furthermore, immune infiltration studies indicated the therapeutic potential of inhibiting the complement system (C4A, C4B) in Age 2 (≥45) patients, providing a potential clinical strategy for USD.

This study illustrated the pathogenesis of USD formation and the diverse characteristics of USD patients with different ages, enhancing our understanding of the disease’s pathogenesis and providing a valuable resource for USD treatment.