Benign prostatic hyperplasia: age-related tissue-remodeling.

Area of Science:

• Urology
• Gerontology
• Cell Biology

Background:

• Benign prostatic hyperplasia (BPH) and enlargement (BPE) are common in aging men, causing lower urinary tract symptoms (LUTS).
• Aging and androgens are primary risk factors, but BPH pathogenesis remains incompletely understood.
• BPH involves nodular overgrowth in the prostate's transition zone, affecting nearly all men by their ninth decade.

Purpose of the Study:

• To review the multifactorial nature of prostate tissue remodeling in elderly men with symptomatic BPH.
• To focus on changes in cell-cell interactions and cell functions within the aging human prostate.
• To synthesize current understanding of BPH pathogenesis.

Main Methods:

• Literature review summarizing proposed theories and implicated mechanisms in BPH.
• Analysis of prostate tissue remodeling characteristics.
• Focus on cellular and molecular changes in the aging prostate.

Main Results:

• Prostate remodeling involves hypertrophic basal cells, altered luminal secretions, inflammation, and increased ROS production.
• Increased bFGF and TGF-beta 1 contribute to stromal proliferation and extracellular matrix production.
• Altered autonomic innervation and neuroendocrine cell function also play roles in BPH development.

Conclusions:

• BPH pathogenesis is multifactorial, involving complex interactions between endocrine, immune, and local cellular mechanisms.
• Cell-cell interactions and altered cell functions are critical in the aging prostate's tissue remodeling.
• Further research into these mechanisms may lead to better management of LUTS associated with BPH.