Mechanisms of prostatic inflammation-mediated male lower urinary tract symptoms
Abstract
Lower urinary tract dysfunction (LUTD) is prevalent in aging men. It is characterized by urinary symptoms such as weak stream and more frequent urination, and is linked to a variety of prostate and urethral pathologies. While the leading medical therapies for male LUTD aim to reduce the tone and volume of the prostate and urethra, no current therapies target two prominent emerging mechanisms of male LUTD: prostate inflammation and fibrosis. LUTD arises and progresses over decades of a man's life, making it difficult to pinpoint disease mechanisms. Non-human research models, including mice, have been useful for investigating slow-progressing diseases of aging. Research involving mouse models of lower urinary tract dysfunction is surging due to a growing suite of genetic, pharmacological and immune-based tools for manipulating mouse prostate histopathology, cell signaling and phenotyping mouse urinary voiding. Current research is focused on understanding how macrophages, fibrocytes, mast cells and other cells are recruited to the prostate and how these cells are activated to drive prostate inflammation and fibrosis. This review highlights recent mouse studies to investigate the cellular and molecular underpinnings of prostate inflammation and fibrosis, and the molecular mechanisms that have emerged from these studies as potential therapeutic targets.
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