Cellular Stress and Molecular Responses in Bladder Ischemia.
Cellular Stress and Molecular Responses in Bladder Ischemia.
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DOI：
10.3390/ijms222111862
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发表时间：
2021-11-01
影响因子：
5.6
通讯作者：
Azadzoi KM
中科院分区：
文献类型：
--
作者：
Yang JH;Choi HP;Niu W;Azadzoi KM
膀胱缺血作为逼尿肌过度活动和下尿路症状（LUTS）的一个促进因素的概念正在发展。盆腔动脉粥样硬化引起的膀胱缺血首先在实验模型中被证实，后来在老年LUTS患者中也被证实。结果表明，早期中度缺血引起逼尿肌过度活动，而长期严重缺血引起的变化与逼尿肌活动不足一致。最近的研究表明，细胞能量传感器、细胞应激传感器和应激反应分子在膀胱缺血反应中起着核心作用。细胞能量传感器腺苷单磷酸活化蛋白激酶在膀胱缺血逼尿肌过度活动和神经退行性变中发挥作用。细胞应激传感器凋亡信号调节激酶1和caspase-3以及热休克蛋白被认为是膀胱缺血时平滑肌结构改变和凋亡反应的重要因素。下游通路似乎包括缺氧诱导因子、转化生长因子β、血管内皮生长因子和神经生长因子。膀胱缺血的分子反应与差异蛋白表达、非编码氨基酸的积累、收缩蛋白和应激反应分子的翻译后修饰有关。进一步了解膀胱缺血的细胞应激反应可能为LUTS提供新的诊断和治疗靶点。
The concept of bladder ischemia as a contributing factor to detrusor overactivity and lower urinary tract symptoms (LUTS) is evolving. Bladder ischemia as a consequence of pelvic arterial atherosclerosis was first documented in experimental models and later in elderly patients with LUTS. It was shown that early-stage moderate ischemia produces detrusor overactivity, while prolonged severe ischemia provokes changes consistent with detrusor underactivity. Recent studies imply a central role of cellular energy sensors, cellular stress sensors, and stress response molecules in bladder responses to ischemia. The cellular energy sensor adenosine monophosphate-activated protein kinase was shown to play a role in detrusor overactivity and neurodegeneration in bladder ischemia. The cellular stress sensors apoptosis signal-regulating kinase 1 and caspase-3 along with heat shock proteins were characterized as important contributing factors to smooth muscle structural modifications and apoptotic responses in bladder ischemia. Downstream pathways seem to involve hypoxia-inducible factor, transforming growth factor beta, vascular endothelial growth factor, and nerve growth factor. Molecular responses to bladder ischemia were associated with differential protein expression, the accumulation of non-coded amino acids, and post-translational modifications of contractile proteins and stress response molecules. Further insight into cellular stress responses in bladder ischemia may provide novel diagnostic and therapeutic targets against LUTS.
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