Title:Current Understanding of Androgen Signaling in Prostatitis and its
Treatment: A Review
Volume: 31
Issue: 27
关键词:
前列腺疾病，目前的治疗，5α-还原酶抑制剂，前列腺炎，前列腺液，锌转运蛋白，丙酮酸转运蛋白。
摘要: Chronic prostatitis is a highly prevalent condition that significantly impacts
the quality of life and fertility of men. Because of its heterogeneous nature, there is no
definitive treatment, which requires ongoing research into its etiology. Additionally, the
association between prostatitis and an elevated risk of prostate cancer highlights the importance
of comprehending androgen involvement in prostatitis. This paper examines
the current understanding of androgen signaling in prostatitis and explores contemporary
therapeutic approaches. It was reviewed Medline articles comprehensively, using
keywords such as nonbacterial prostatitis, prostatitis infertility, androgen role in prostatitis,
and chronic pelvic pain. Several cellular targets are linked to androgen signaling.
Notably, the major tyrosine phosphatase activity (cPAcP) in normal human prostate is influenced
by androgen signaling, and its serum levels inversely correlate with prostate
cancer progression. Androgens also regulate membrane-associated zinc and pyruvate
transporters transduction in prostate cells, suggesting promising avenues for novel drug
development aimed at inhibiting these molecules to reduce cancer tumor growth. Various
therapies for prostatitis have been evaluated, including antibiotics, anti-inflammatory
medications (including bioflavonoids), neuromodulators, alpha-blockers, 5α-reductase
inhibitors, and androgen receptor antagonists. These therapies have demonstrated
varying degrees of success in ameliorating symptoms.In conclusion, aging decreases circulating
T and intraprostatic DHT, altering the proper functioning of the prostate, reducing
the ability of androgens to maintain normal Zn2+ levels, and diminishing the secretion
of citrate, PAcP, and other proteins into the prostatic fluid. The Zn2+-transporter decreases
or is absent in prostate cancer, so the pyruvate transporter activates. Consequently,
the cell ATP increases, inducing tumor growth.
