전립선 비대증의 분자, 내분비적 기전 Molecular and endocrine basis of the development of benign prostatic hyperplasia
- 최초 등록일
- 2019.06.20
- 최종 저작일
- 2019.05
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MS 워드
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목차
1. Hormonal regulation
1) Androgens Pathway
2) Estrogens
2. Regulation of Programmed Cell Death (apoptosis)
3. Stromal-Epithelial Interaction
4. Growth Factors
5. Other signaling pathways
6. Inflammatory Pathways and Cytokines
본문내용
Histopathologically, BPH is defined as an increased number of epithelial and stromal cells in the periurethral area of the prostate and referred to as hyperplasia. Androgens, estrogens, stromal-epithelial interactions, growth factors, regulation of programmed cell death and neurotransmitters may play a role, either singly or in combination, in the etiology of the hyperplastic process.
1. Hormonal regulation
1) Androgens Pathway
The development of BPH requires the presence of testicular androgens during prostate development, puberty, and aging. Prostatic levels of dihydrotestosterone (DHT) as well as the androgen recep¬tor (AR) remain high with aging despite the peripheral levels of testosterone are decreasing. Androgen with¬drawal leads to partial involution of established BPH. However, there is no clear relationship between the concentration of androgens and prostate size in aging men. In the prostate, the nuclear membrane–bound enzyme steroid 5α-reductase converts the hormone testosterone
참고 자료
Campbell-Walsh Urology, chapter 103.
Madersbacher, S., Sampson, N., & Culig, Z. (2019). Pathophysiology of Benign Prostatic Hyperplasia and Benign Prostatic Enlargement: A Mini-Review. Gerontology, 1-7.
Lee, K. L., & Peehl, D. M. (2004). Molecular and cellular pathogenesis of benign prostatic hyperplasia. The Journal of urology, 172(5), 1784-1791.
