Phua Teow J
Molecular Medicine, NSW Health Pathology, John Hunter Hospital, Newcastle, NSW 2305, Australia.
Medicines (Basel). 2021 Jun 11;8(6):30. doi: 10.3390/medicines8060030.
The etiology of benign prostatic hyperplasia and prostate cancer are unknown, with ageing being the greatness risk factor.
This new perspective evaluates the available interdisciplinary evidence regarding prostate ageing in terms of the cell biology of regulation and homeostasis, which could explain the timeline of evolutionary cancer biology as degenerative, inflammatory and neoplasm progressions in these multifactorial and heterogeneous prostatic diseases.
This prostate ageing degeneration hypothesis encompasses the testosterone-vascular-inflamm-ageing triad, along with the cell biology regulation of amyloidosis and autophagy within an evolutionary tumorigenesis microenvironment.
An understanding of these biological processes of prostate ageing can provide potential strategies for early prevention and could contribute to maintaining quality of life for the ageing individual along with substantial medical cost savings.
良性前列腺增生和前列腺癌的病因尚不清楚，老龄化是最大的风险因素。
这一新观点从调节和体内平衡的细胞生物学角度评估了有关前列腺老化的现有跨学科证据，这可以解释在这些多因素和异质性前列腺疾病中，作为退行性、炎症性和肿瘤进展的进化性癌症生物学的时间线。
这种前列腺老化退化假说涵盖了睾酮-血管-炎症-老化三联征，以及在进化性肿瘤发生微环境中淀粉样变性和自噬的细胞生物学调节。
了解前列腺老化的这些生物学过程可为早期预防提供潜在策略，并有助于维持老年人的生活质量，同时大幅节省医疗成本。
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