良性前列腺增生（BPH) 是老年男性最常见的疾病之一, 严重影响患者的身心健康和生活质量。研究表明，缺氧作为BPH的致病因素之一，能诱导前列腺基质细胞自噬，而自噬在细胞增殖、生长因子调控中发挥重要作用，但其具体机制尚不清楚。文献报道和课题组前期研究显示：低氧诱导前列腺基质细胞的HIF-1α表达上调，并活化自噬通路中的信号蛋白LC3；低氧促进该细胞释放转化生长因子β1）和成纤维生长因子2/7，导致前列腺基质细胞的增殖分化。这些结果提示：低氧可能通过激活内质网应激导致自噬增强，从而促进转化生长因子β1和成纤维生长因子2/7释放，最终导致BPH。本课题研究缺氧诱导的前列腺基质细胞自噬变化，以及自噬对基质细胞增殖分化的影响，并在动物模型中加以验证，探讨“低氧、自噬与增生”的调节模式，以期阐明HIF-1α在缺氧诱导的前列腺基质细胞自噬调节与增殖分化发生的机制，为寻找治疗BPH提供理论依据和治疗策略。

Benign prostatic hyperplasia (BPH) as one of the most common diseases in elderly men, can seriously affect the health of patients. Previous studies have shown that hypoxia as one causative factor for BPH, can induce autophagy in prostate stromal cells, which play crucial roles in the regulation of cell proliferation and growth factors, but the exact mechanism is unclear. Previous studies and our results showed that hypoxia could increase expression of HIF-1α and activate autophagy, and autophagy mediate the release of transforming growth factor β1 (TGF-β1) and fibroblast growth factor 2/7, which could result in the proliferation and differentiation of prostate stromal cells. Through up or down regulating the expression of HIF-1α and autophagy in cell and animal models with hypoxia, the present reserch tries to detect BPH and its signaling pathway with Western blot/electron microscopy/confocal laser microscope in prostate stromal cells, to explore the model of " hypoxia , autophagy and proliferation ". We intend to clarify the mechanism that HIF-1α regulates autophagy induced by hypoxia in prostate stromal cells, and provide a theoretical basis for an effective treatment to BPH.