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间质性膀胱炎/疼痛性膀胱综合征中的细胞信号传导

Cell signaling in interstitial cystitis/painful bladder syndrome.

作者信息

Keay Susan

机构信息

Department of Medicine, University of Maryland School of Medicine and Veterans Administration Maryland Health Care System, Baltimore, Maryland, United States.

出版信息

Cell Signal. 2008 Dec;20(12):2174-9. doi: 10.1016/j.cellsig.2008.06.004. Epub 2008 Jun 19.

Abstract

Evidence for several types of cell signaling abnormalities has been presented for patients with interstitial cystitis/painful bladder syndrome (IC/PBS), a poorly understood chronic painful bladder disorder for which currently there is no reliable effective therapy. Increases or decreases in various urine cytokines and growth factors have been found in patient specimens, along with abnormal expression of epithelial differentiation markers, growth factors, cell membrane proteins, neurotransmitters, and other cytokines in tissue biopsies and/or explanted bladder cells from IC/PBS patients. Some of the abnormalities found in bladder epithelial cells from IC/PBS patients have been shown to be induced in normal cells by an antiproliferative factor from IC/PBS bladder epithelial cells that binds to a functional cell membrane receptor (CKAP4/p63). Greater understanding of cell signaling events associated with this debilitating disorder may lead to the development of more effective therapies.

摘要

对于间质性膀胱炎/膀胱疼痛综合征(IC/PBS)患者,已有证据表明存在多种类型的细胞信号异常。IC/PBS是一种了解甚少的慢性膀胱疼痛疾病,目前尚无可靠的有效治疗方法。在患者样本中发现各种尿液细胞因子和生长因子增加或减少,同时在IC/PBS患者的组织活检和/或体外培养的膀胱细胞中,上皮分化标志物、生长因子、细胞膜蛋白、神经递质和其他细胞因子也存在异常表达。已证明,IC/PBS患者膀胱上皮细胞中发现的一些异常可由IC/PBS膀胱上皮细胞的抗增殖因子在正常细胞中诱导产生,该因子与功能性细胞膜受体(CKAP4/p63)结合。对与这种使人衰弱的疾病相关的细胞信号事件有更深入的了解,可能会带来更有效的治疗方法。

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