{"title":"Transforming growth factors and insulin-like growth factors in chronic kidney disease","authors":"R. Mak, W. Cheung","doi":"10.1080/17471060701486225","DOIUrl":null,"url":null,"abstract":"Irrespective of its primary etiology, chronic kidney disease (CKD) progresses. Glomerulosclerosis, interstitial fibrosis, and tubular atrophy are key features of CKD. The important roles of the transforming growth factor (TGF) and insulin-like growth factor (IGF) superfamilies have been indicated in recent studies. This review provides an update of the literature on these factors and their interactions in the pathophysiology of the progression of CKD as well as cachexia, which is an important complication. Specifically, the functions of key molecules, such as TGF-β, bone morphogenetic protein-7, myostatin, relaxin, and IGF-I in the pathobiology underlying CKD progression and CKD-associated cachexia are discussed.","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"26 1","pages":"59-64"},"PeriodicalIF":0.0000,"publicationDate":"2009-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of organ dysfunction","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/17471060701486225","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 2
Abstract
Irrespective of its primary etiology, chronic kidney disease (CKD) progresses. Glomerulosclerosis, interstitial fibrosis, and tubular atrophy are key features of CKD. The important roles of the transforming growth factor (TGF) and insulin-like growth factor (IGF) superfamilies have been indicated in recent studies. This review provides an update of the literature on these factors and their interactions in the pathophysiology of the progression of CKD as well as cachexia, which is an important complication. Specifically, the functions of key molecules, such as TGF-β, bone morphogenetic protein-7, myostatin, relaxin, and IGF-I in the pathobiology underlying CKD progression and CKD-associated cachexia are discussed.