细胞粘附分子与肾脏疾病

细胞粘附分子与肾脏疾病刘俊综述王小宁审校细胞粘附分子（ＣＡＭｓ）是一类能介导细胞间粘附以及细胞与细胞外基质粘附的糖蛋白。其种类繁多，作用极广泛，在炎症反应、免疫识别、特别是免疫细胞间的相互作用中起重要作用，还参与跨膜信号的传递［１］。最近，ＣＡＭｓ介...     

细胞粘附分子与肾脏疾病

粘附分子是介导细胞与细胞，细胞与细胞外基质粘附的一类配基或受体，细胞粘附对细胞分化组织器官的分化，免疫细胞的激活和免疫细胞间的相互作用、白细胞的再循环和迁移、以及肿瘤细胞的生长和扩散都起着重要的基本作用，在过去的十年里，粘附分子的研究进展有极其迅速，除了粘附分子的三个经典家族外，最近还报导了一类化学吸引的细胞因子，称为化学增活素，粘附分子在肾组织的表达；粘附分子在肾炎中的表达变化；抗粘附分子的单克     

肾脏疾病细胞凋亡

细胞凋亡参与肾脏正常发育及肾疾病发生等多个过程，在肾脏疾病的发生发展过程中发挥着益或有害的作用，探讨细胞凋亡在肾疾病中的作用是近年来研究的热点之一，本文就细胞凋亡在其相关肾脏疾病中的作用作一综述。     

肾脏细胞凋亡的分子机理研究进展

凋亡与增殖是调控细胞数目趋态的，作用相反的一对机制，细胞凋亡与肾脏疾病的发生，发展及转归均密切相关，本文综述了参与细胞凋亡的信号分子以及肾脏细胞凋亡领域的研究进展。     

细胞周期调节蛋白与肾脏疾病

细胞周期调节蛋白按其作用分为细胞周期正控蛋白与负控蛋白。前者包括周期素（ｃｙｃｌｉｎＡ～Ｈ）、周期素依赖性激酶（ＣＤＫ２～ＣＤＫ７）、视网膜母细胞瘤（ｐＲｂ）等；后者总称周期素激酶抑制剂（ＣＫＩ），由ＣＩＰ／ＫＩＰ家族（含ｐ２１、ｐ２７、ｐ５７）和ＩＮＫ４家族（ｐ１５、ｐ１６、ｐ１８、ｐ１９）组成。ｃｙｃｌｉｎ与ＣＤＫ结合成多种活性复合物，使ｐＲｂ等下游蛋白磷酸化而发挥其正控作用；ＣＫＩ抑制ｃｙｃｌｉｎ－ＣＤＫ的活性而起到负控作用。在各种肾脏疾病中，多种因素影响肾小球细胞的增生或肥大，其主要机制与细胞周期调节蛋白有关     

成纤维细胞生长因子-23在肾脏疾病中的作用

本文综述了FGF-23的结构、生化特性及其在肾脏病中的作用.     

活性氧对膀胱癌树突状细胞调节的研究

我们通过细胞培养方法观察外源性活性氧自由基一氧化氮（NO）、羟自由基对膀胱癌患者树突状细胞（DC）刺激自体淋巴细胞增殖及对DC诱导细胞毒性T细胞（CTLs）杀伤膀胱癌细胞株T-24的影响，了解NO、羟自由基对DC递呈抗原功能的影响。现报告如下。     

肾脏细胞的活化与慢性进展性肾病

慢性肾脏疾病常以不同的方式、速度发展，直致终末期肾功能衰竭。近年来由于细胞分子生物学技术的发展，对肾脏细胞生物学研究的深入起到了推动性作用。从而证实肾脏细胞的活化对进展性肾病的发生、发展有着重要的影响。肾脏细胞成分包括固有细胞如肾小球上皮细胞、内皮细胞、系膜细胞。肾小管上皮细胞、肾间质成纤维细胞。这些细胞在慢性进展性肾病中不但是受害的靶细胞，而且通过细胞活化产生多种细胞因子、生长因子等活跃的参与疾病的发展过程、它们可以直接合成细胞外基质（ＥＣＭ），也能够产生蛋白酶调节 ＥＣＭ的代谢。由外界浸润的…     

Fas和细胞凋亡与肾脏疾病

细胞凋亡是机体维持自稳态和免疫系统正常发育的重要机制；也是肾脏发生，发育及肾脏疾病的病理损伤与修复过程中必不可少的环节，Ｆａｓ系统不仅参与肾小球损伤过程中肾细胞的凋亡，也参与急性肾移植的排斥。此外，系统性红斑狼疮及狼疮性肾炎的发展与Ｆａｓ功能缺陷相关。     

Fas和细胞凋亡与肾脏疾病

细胞凋亡是机体维持自稳态和免疫系统正常发育的重要机制,也是肾脏发生、发育及肾脏疾病的病理损伤与修复过程中必不可少的环节,Ｆａｓ系统不仅参与肾小球损伤过程中肾细胞的凋亡,也参与急性肾移植的排斥。此外,系统性红斑狼疮及狼疮性肾炎的发展与Ｆａｓ功能缺陷相关     

Autophagy: a novel therapeutic target for kidney diseases

Autophagy meaning ??self-eating?? in Greek, is a large-scale mechanism of intracellular degradation that seeks to maintain homeostasis in cells of all eukaryotes, from yeast to humans. Over the past several decades, autophagy research has actively proceeded both at home and abroad. As a result, studies have reported the physiological role of autophagy in different organs of mammals and of the role that impairment of its activation plays in the development of age-related diseases, abnormal glucose?Clipid metabolism, and neurodegenerative disorders. Currently, new therapies targeting the regulation of activation of autophagy are anticipated, and research is continuing. In recent years, the role of autophagy in the kidneys has gradually been elucidated, and reports are indicating an association between autophagy and the development of various kidney diseases. This paper reviews the molecular mechanisms regulating autophagy and discusses new findings from autophagy research on the kidney and issues that have yet to be resolved.     

Chemokines: new target molecules in renal diseases

The presence of leukocytes in the diseased kidneys is a hallmark of almost any kind of renal disease. Activated leukocytes are implicated in playing a crucial role in the pathogenesis of renal diseases. Recent investigations of the pathophysiological roles of chemokines and their cognate receptors have shed light on the detailed molecular mechanisms of leukocyte trafficking and activation in the diseased kidneys. This study summarizes findings that: (1) chemokine/chemokine receptor systems may be essentially involved in the pathogenesis of phase-specific renal disorders, (2) the measurement of urinary levels of chemokines may be clinically useful for monitoring different disease phases and activities in human renal diseases, and (3) interventions in chemokine/chemokine receptor systems may have potential as particular immunotherapeutic strategies to combat specific phases of renal diseases. Further investigations of anti-chemokine therapies for renal diseases will be required before clinical application is feasible. Received: May 22, 2000 / Accepted: June 28, 2000     

Peritubular capillary rarefaction: a new therapeutic target in chronic kidney disease

Chronic kidney disease (CKD) has reached worldwide epidemic proportions and desperately needs new therapies. Peritubular capillary (PTC) rarefaction, together with interstitial fibrosis and tubular atrophy, is one of the major hallmarks of CKD and predicts renal outcome in patients with CKD. PTC endothelial cells (ECs) undergo apoptosis during CKD, leading to capillary loss, tissue hypoxia, and oxidative stress. Although the mechanisms of PTC rarefaction are not well understood, the process of PTC rarefaction depends on multiple events that occur during CKD. These events, which lead to an antiangiogenic environment, include deprivation of EC survival factors, increased production of vascular growth inhibitors, malfunction of ECs, dysfunction of endothelial progenitor cells, and loss of EC integrity via pericyte detachment from the vasculature. In this review, we focus on major factors regulating angiogenesis and EC survival and describe the roles of these factors in PTC rarefaction during CKD and possible therapeutic applications.     

Chemokine receptor CCR1: a new target for progressive kidney disease

Infiltrating leukocytes are thought to contribute to the progression of kidney disease. Locally produced chemokines guide circulating leukocytes into the kidney, which renders therapeutic blockade of respective chemokine receptors on the leukocyte surface as potential targets for the inhibition of renal leukocyte recruitment. By using mutant mice and specific antagonists, we found that chemokine receptor CCR1 has non-redundant functions for leukocyte adhesion to activated vascular endothelium and for transendothelial diapedesis. Most importantly, CCR1 blockade with a specific small molecule antagonist can improve injury in several types of progressive kidney disease models, even if treatment is initiated in advanced disease states. Identification of new targets may add to the therapeutic options in chronic kidney disease.     

Dendritic cells as a target of immunosuppressive drugs

For a long time, it has been recognized that dendritic cells (DCs) play a pivotal role in the induction of immune responses, including alloimmunity. More recently, it has become clear that DCs are also central players in the other extreme end of immune regulation (ie, tolerance induction). Initially, it was proposed that different DC lineages might be responsible for these different activities. However, in addition, the differentiation/maturation stage of DCs determines its functional capacity. In recent years, it has been shown that several pharmacological agents have the capacity to control or direct these DC functions. In the present review, we will give an overview of these findings and especially discuss these in the view of strategies to induce allospecific tolerance in transplantation.     

Dendritic cells in the kidney

Dendritic cells (DC) in nonlymphoid organs function at the crossroads of innate and adaptive immunity, self-tolerance, and tissue homeostasis. This review provides an overview of the study of DC in the kidney, tracing its history leading to the current knowledge of the origins, migration, and function of renal DC. Together, these studies suggest that renal DC play a critical role in the health and disease of the kidney, opening the way to direct targeting of renal DC for therapeutic benefit.     

Dendritic cells: not just another cell type in the kidney, but a complex immune sentinel network

Dendritic cells (DCs) are crucial for inducing and regulating adaptive immunity. These cells also exist in the kidney, where, however, their function had been unknown. A study by Soos et al. now demonstrates that renal DCs form an intricate cellular network that continuously surveys the tubulointerstitium, and reveals a previously unrecognized immune sentinel system of the kidney.