Benign prostat hiperplazisi (BPH) ve apopitozis

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.

Benign prostatic hyperplasia (BPH) and apoptosis

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.

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