{"title":"HSP70家族在肾脏炎症反应中的作用。","authors":"Walter Manucha","doi":"10.2174/1871528113666140805125632","DOIUrl":null,"url":null,"abstract":"<p><p>Heat shock proteins (HSP) are a shock induced family of proteins, whose most prominent members are a group of molecules dedicated to maintaining the function of other proteins. Interestingly, after being exposed to heat shock typical proinflammatory agonists modify the heat shock-induced transcriptional program and expression of HSP genes, suggesting a complex reciprocal regulation between the inflammatory pathway and that of the heat shock response. The specific task of Heat shock protein 70 (Hsp 70), the most widespread and highly conserved HSP, is to protect against inflammation through multiple mechanisms. So, the expression of immune reactivity to Hsp70 in the kidney could be a cause of hypertension. Hsp70 modulates inflammatory response, as well as down-regulates the nuclear factor kappa-lightchain- enhancer of activated B cells. Also, a decreased expression of renal Hsp70 may contribute to activate the toll-like receptor 4-initiating inflammatory signal pathway. In addition, several studies have revealed that Hsp70 is involved in the regulation of Angiotensin II, a peptide with proinflammatory activity. Increased inflammatory response is generated by nicotinamide adenine dinucleotide phosphate oxidase, following activation by Angiotensin II. Interestingly, Hsp70 protects the renal epithelium by modulation of nicotinamide adenine dinucleotide phosphate oxidase, a fundamental step in the pro-inflammatory mechanism. This article aims to summarize our understanding about possible mechanisms improving the renal inflammatory process linked to Hsp70 expression. Finally, from a therapeutic point of view, the notion of antiinflammatory tools regulating Hsp70 could directly affect the inflammatory renal disease. </p>","PeriodicalId":13680,"journal":{"name":"Inflammation & allergy drug targets","volume":"13 4","pages":"235-40"},"PeriodicalIF":0.0000,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"12","resultStr":"{\"title\":\"HSP70 Family in the Renal Inflammatory Response.\",\"authors\":\"Walter Manucha\",\"doi\":\"10.2174/1871528113666140805125632\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Heat shock proteins (HSP) are a shock induced family of proteins, whose most prominent members are a group of molecules dedicated to maintaining the function of other proteins. Interestingly, after being exposed to heat shock typical proinflammatory agonists modify the heat shock-induced transcriptional program and expression of HSP genes, suggesting a complex reciprocal regulation between the inflammatory pathway and that of the heat shock response. The specific task of Heat shock protein 70 (Hsp 70), the most widespread and highly conserved HSP, is to protect against inflammation through multiple mechanisms. So, the expression of immune reactivity to Hsp70 in the kidney could be a cause of hypertension. Hsp70 modulates inflammatory response, as well as down-regulates the nuclear factor kappa-lightchain- enhancer of activated B cells. Also, a decreased expression of renal Hsp70 may contribute to activate the toll-like receptor 4-initiating inflammatory signal pathway. In addition, several studies have revealed that Hsp70 is involved in the regulation of Angiotensin II, a peptide with proinflammatory activity. Increased inflammatory response is generated by nicotinamide adenine dinucleotide phosphate oxidase, following activation by Angiotensin II. Interestingly, Hsp70 protects the renal epithelium by modulation of nicotinamide adenine dinucleotide phosphate oxidase, a fundamental step in the pro-inflammatory mechanism. This article aims to summarize our understanding about possible mechanisms improving the renal inflammatory process linked to Hsp70 expression. Finally, from a therapeutic point of view, the notion of antiinflammatory tools regulating Hsp70 could directly affect the inflammatory renal disease. </p>\",\"PeriodicalId\":13680,\"journal\":{\"name\":\"Inflammation & allergy drug targets\",\"volume\":\"13 4\",\"pages\":\"235-40\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2014-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"12\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Inflammation & allergy drug targets\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2174/1871528113666140805125632\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Inflammation & allergy drug targets","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/1871528113666140805125632","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 12
摘要
热休克蛋白(HSP)是一个休克诱导蛋白家族,其最重要的成员是一组致力于维持其他蛋白质功能的分子。有趣的是,在暴露于热休克后,典型的促炎激动剂会改变热休克诱导的转录程序和热休克基因的表达,这表明炎症途径和热休克反应之间存在复杂的相互调节。热休克蛋白70 (Heat shock protein 70, hsp70)是一种分布最广且高度保守的热休克蛋白,其具体任务是通过多种机制来预防炎症。所以肾脏中对Hsp70的免疫反应性表达可能是高血压的一个原因。Hsp70调节炎症反应,下调活化B细胞的核因子kappa-轻链增强子。此外,肾脏Hsp70表达的降低可能有助于激活toll样受体4启动炎症信号通路。此外,一些研究表明,Hsp70参与调节血管紧张素II,一种具有促炎活性的肽。血管紧张素II激活后,烟酰胺腺嘌呤二核苷酸磷酸氧化酶引起炎症反应增加。有趣的是,Hsp70通过调节烟酰胺腺嘌呤二核苷酸磷酸氧化酶来保护肾上皮,这是促炎机制的一个基本步骤。本文旨在总结我们对改善与Hsp70表达相关的肾脏炎症过程的可能机制的理解。最后,从治疗的角度来看,调节Hsp70的抗炎工具的概念可以直接影响炎症性肾脏疾病。
Heat shock proteins (HSP) are a shock induced family of proteins, whose most prominent members are a group of molecules dedicated to maintaining the function of other proteins. Interestingly, after being exposed to heat shock typical proinflammatory agonists modify the heat shock-induced transcriptional program and expression of HSP genes, suggesting a complex reciprocal regulation between the inflammatory pathway and that of the heat shock response. The specific task of Heat shock protein 70 (Hsp 70), the most widespread and highly conserved HSP, is to protect against inflammation through multiple mechanisms. So, the expression of immune reactivity to Hsp70 in the kidney could be a cause of hypertension. Hsp70 modulates inflammatory response, as well as down-regulates the nuclear factor kappa-lightchain- enhancer of activated B cells. Also, a decreased expression of renal Hsp70 may contribute to activate the toll-like receptor 4-initiating inflammatory signal pathway. In addition, several studies have revealed that Hsp70 is involved in the regulation of Angiotensin II, a peptide with proinflammatory activity. Increased inflammatory response is generated by nicotinamide adenine dinucleotide phosphate oxidase, following activation by Angiotensin II. Interestingly, Hsp70 protects the renal epithelium by modulation of nicotinamide adenine dinucleotide phosphate oxidase, a fundamental step in the pro-inflammatory mechanism. This article aims to summarize our understanding about possible mechanisms improving the renal inflammatory process linked to Hsp70 expression. Finally, from a therapeutic point of view, the notion of antiinflammatory tools regulating Hsp70 could directly affect the inflammatory renal disease.