
膀胱尿路上皮细胞焦亡在间质性膀胱炎发病机制及其病理生理表现中的研究进展
庞磊, 双卫兵
膀胱尿路上皮细胞焦亡在间质性膀胱炎发病机制及其病理生理表现中的研究进展
Research advances in the pathogenesis and pathophysiological manifestations of interstitial cystitis caused by urothelial cell pyroptosis
细胞焦亡是一种由炎症小体介导的、程序性的促炎症性细胞死亡方式,可以导致细胞内非活性细胞因子的激活以及消皮素D(gasdermin D,GSDMD)的裂解。炎症性膀胱疾病的主要病理结局是膀胱的顺应性丧失,而细胞焦亡在其过程中起到了重要的作用。一些研究发现,细胞焦亡受到DNA甲基化、线粒体DNA氧化损伤等机制的调控,从而干预间质性膀胱炎中膀胱尿路上皮细胞的生物学行为,从而诱发膀胱顺应性损伤。因此,通过概述间质性膀胱炎中细胞焦亡的调节机制以及焦亡在炎症性膀胱疾病中的潜在作用,以探索间质性膀胱炎的潜在诊断标志物,有助于间质性膀胱炎的预防和治疗。
Pyroptosis is a proinflammatory form of regulated cell death that can lead to the activation of inactive cytokines and the cleavage of gasdermin D in cells. The main pathological outcome of inflammatory bladder disease is the loss of bladder compliance,and cell pyroptosis plays an important role in this process. Some studies have shown that cell pyroptosis is regulated by various mechanisms such as DNA methylation and mitochondrial DNA oxidative damage,which intervene in the biological behavior of bladder urothelial cells in interstitial cystitis and induce impairment of bladder compliance. Therefore,this article reviews the regulatory mechanisms of cell pyroptosis in interstitial cystitis and the potential role of pyroptosis in inflammatory bladder diseases,in order to explore potential diagnostic biomarkers for interstitial cystitis and facilitate the prevention and treatment of interstitial cystitis.
间质性膀胱炎 / 细胞焦亡 / DNA甲基化 / 线粒体氧化损伤
interstitial cystitis / pyroptosis / DNA methylation / mitochondrial oxidative damage
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