Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota.
J Am Soc Nephrol. 2014 Jan;25(1):18-32. doi: 10.1681/ASN.2013040398. Epub 2013 Dec 12.
Polycystic kidney disease (PKD) is a leading cause of ESRD worldwide. In PKD, excessive cell proliferation and fluid secretion, pathogenic interactions of mutated epithelial cells with an abnormal extracellular matrix and alternatively activated interstitial macrophages, and the disruption of mechanisms controlling tubular diameter contribute to cyst formation. Studies with animal models suggest that several diverse pathophysiologic mechanisms, including dysregulation of intracellular calcium levels and cAMP signaling, mediate these cystogenic mechanisms. This article reviews the evidence implicating calcium and cAMP as central players in a network of signaling pathways underlying the pathogenesis of PKD and considers the therapeutic relevance of treatment strategies targeting cAMP signaling.
多囊肾病 (PKD) 是全球导致终末期肾病 (ESRD) 的主要原因。在 PKD 中,过度的细胞增殖和液体分泌、突变上皮细胞与异常细胞外基质的病理性相互作用以及对控制管腔直径的机制的破坏导致囊肿形成。动物模型研究表明,包括细胞内钙水平和 cAMP 信号转导失调在内的几种不同的病理生理机制,介导了这些囊肿形成机制。本文综述了钙和 cAMP 作为多囊肾病发病机制相关信号通路网络中关键因子的证据,并考虑了靶向 cAMP 信号转导的治疗策略的治疗相关性。