Journals / Ankara Üniversitesi Tıp Fakültesi Mecmuası / 2006 / Cilt: 59 - Sayı: 3

Benign prostatic hyperplasia (BPH) and apoptosis

Benign prostat hiperplazisi (BPH) ve apopitozis

Pages
132–136
Publication Date
2022-10-10
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Here we reviewed the medical therapies of BPH and their apoptotic effects.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Apoptosis is defined as programmed cell death.
📊
Key Findings & Data:Medical treatment of benign prostate hyperplasia (BPH) targets relief of symptoms by causing either relaxation of the prostatic smooth muscle with α1 adrenergic blokade, or shrinkage of the gland with 5α-reductase inhibitors.
💡
Conclusion & Impact:Here we reviewed the medical therapies of BPH and their apoptotic effects.
🔬Design:Review & Systematic Survey
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Apoptosis is defined as programmed cell death. Prostate growth and development is under androgenic control, which maintains a balance between cell death and cell proliferation. Studies on the dynamics of prostate growth in BPH indicate that disruption of the molecular mechanisms that regulate apoptosis and cell proliferation among the stroma and epithelial components may underlie the abnormal growth of the gland that characterizes BPH. Medical treatment of benign prostate hyperplasia (BPH) targets relief of symptoms by causing either relaxation of the prostatic smooth muscle with α1 adrenergic blokade, or shrinkage of the gland with 5α-reductase inhibitors. Out of their primary effect, both α1 adrenergic blockers and 5α-reductase inhibitors induce apoptosis in the prostate gland. Here we reviewed the medical therapies of BPH and their apoptotic effects.

Özet

Apopitozis programlanmış hücre ölümü olarak tanımlanır. Prostat büyümesi ve gelişmesi, hücre ölümü ve proliferasyonu arasında denge sağlayan androjenik kontrolün etkisi altındadır. BPH’daki prostat büyümesini inceleyen çalışmalar; stroma ve epitelyal komponentler arasındaki hücre proliferasyonu ve apopitozis dengesini sağlayan moleküler mekanizmalarda oluşan bozukluğun BPH ile karakterize anormal glands büyümesinin altında yatan sebep olduğunu göstermektedir. BPH’nın medikal tedavisi, α1 adrenoreseptör (AR) blokörlerinin prostatik düz kasların relaksasyonuna bağlı veya 5α redüktaz inhibitörlerinin glandı küçültmesine bağlı etkileriyle sikayetlerin giderilmesini hedefler. Birincil etki mekanizmaları dışında, α1 adrenoreseptör (AR) blokörlerinin ve 5α redüktaz inhibitörlerinin prostat hücrelerinde apopitozisi de indükledikleri gösterilmiştir. Bu makalede BPH’nın medikal tedavisinde kullanılan ilaçlar ile apopitotik etkileri gözden geçirilmiştir.

🔖

Cite This Article

YURDAKUL, T., GÜVEN, S. (2022). Benign prostatic hyperplasia (BPH) and apoptosis. Ankara Üniversitesi Tıp Fakültesi Mecmuası, Cilt: 59 - Sayı: 3, 132–136. https://ajindex.com/articles/443967

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (16)

  1. . Ziada A, Rosenblum M, Crawford ED. Benign prostatic hyperplasia: an overview. Urology. 1999
  2. Coffey DS. and Walsh PC. Clinical and experimental studies of benign prostatic hyperplasia. Urol Clin North Am. 1990
  3. Yang G, Timme TL, Park SH et al. Transforming growth factor beta 1 transduced mouse prostate reconstitutions: II. Induction of apoptosis by doxazosin. Prostate. 1997
  4. Djakiew D, Dysregulated expression of growth factors and their receptors in the development of prostate cancer: review article. Prostate. 2000
  5. Bartsch G, Muller HR, Oberholzer M et al. Light microscopic stereological analysis of the normal human prostate and of benign prostate hyperplasia. J Urol. 1992
  6. McNeal J, Pathology of benign prostatic hyperplasia. Insight into etiology. Urol Clin North Am. 1990
  7. Kledjian K, Kyprianou N. Anoikis induction by quinazoline based alfa-1 adrenoreceptor antagonists in prostate cancer cells: antagonistic effect of BCL-2. J Urol. 2003
  8. Tahmatzopoulos A, Kyprianou N, Apopitotic impact of alfa-1 blockers on prostate cancer growth: a nyth or an inviting reality? The prostate. 2000
  9. McDonell TJ, Troncoso P, Brisbay SM et al. Expression of the protooncogene bcl-2 in the prostate and its association with emergence of androgen-independent prostate cancer. Cancer Res. 1992
  10. Newton K, Strasser A. The Bcl-2 family and cell death regulation. Curr Opin Genet Dev. 1998
  11. 1, 68-75. 11. Kerr JF, Searle J. Deletion of cells by apoptosis during castrationinduced involution of the rat prostate. Virchows Arch B Cell Pathol. 1973
  12. 25 (13):87-102. 12. Denmeade SR, Lin XS, Isaacs JT. Role of programmed (apoptotic) cell death during the progression and therapy for prostate cancer. Prostate. 1996
  13. 28(4):251-65 13. Shao TC, Kong A, Marafelia P et al. Effects of finasteride on the rat ventral prostate. J Androl. 1993
  14. 14 (2):79-86. 14. Rittmaster RS, Manning AP, Wright AS et al. Evidence for atrophy and apoptosis in the ventral prostate of rats given the 5 alpha-reductase inhibitor finasteride. Endocrinology. 1995
  15. 136 (2):741-8. 15. Wright AS, Thomas LN, Douglas RC et al. Relative potency of testosterone and dihydrotestosterone in preventing atrophy and apoptosis in the prostate of the castrated rat. J Clin Invest. 1996
  16. 98 (11):2558-63. 16. Rittmaster RS, Norman RW, Thomas LN et al. Evidence for atrophy and apoptosis in the prostates of men given fina