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Comment
. 2019 Jun 1;316(6):F1091-F1093.
doi: 10.1152/ajprenal.00102.2019. Epub 2019 Mar 13.

Targeting a fibrotic bottleneck may provide an opening in the treatment of LUTS

William A Ricke  1 , Reginald C Bruskewitz  1 , Teresa T Liu  1
Affiliations
Comment

Targeting a fibrotic bottleneck may provide an opening in the treatment of LUTS

William A Ricke et al. Am J Physiol Renal Physiol. .
No abstract available

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Conflict of interest statement

No conflicts of interest, financial or otherwise, are declared by the authors.

Figures

Fig. 1.
Fig. 1.
Schematic of prostate fibrosis and benign prostatic hyperplasia (BPH)/lower urinary tract symptoms (LUTS). Some factors contributing to the development of fibrosis include infection (2a), metabolic disorders (e.g., type 2 diabetes and obesity), hormones, and aging. These can be interrogated for biomarkers with proteomic and metabolomics tools. The impact of fibrosis on BPH/LUTS must include an understanding of spatial (i.e., cell types) and temporal (progressive remodeling) collagen expression, anatomic location (periurethral vs. diffuse throughout prostate) of collagen expression, and type of collagen (e.g., collagen-1, -2,…-29) and structure (i.e., collagen fiber metrics) within the prostate. The research tools necessary to examine fibrosis include a variety of advanced imaging and staining modalities, including picrosirius red, Masson’s trichrome, PolScope, and multiphoton microscopy. Current treatments for BPH/LUTS [i.e., 5α-reductase inhibitors (5ARIs) and α-blockers] are ineffective at treating fibrosis-mediated disease. Instead, antifibrotic treatments need to be developed using preclinical animal and patient-derived models to prevent or treat fibrosis-mediated BPH/LUTS. IHC, immunohistochemistry; ISH, in situ hybridization.
See this image and copyright information in PMC

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