Document Detail

MicroRNAs in Diabetic Kidney Disease.
MedLine Citation:
PMID:  24550986     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Rapid growth of diabetes and diabetic kidney disease exerts a great burden on society. Owing to the lack of effective treatments for diabetic kidney disease, treatment relies on drugs that either reduces its progression or involve renal replacement therapies, such as dialysis and kidney transplantation. It is urgent to search for biomarkers for early diagnosis and effective therapy. The discovery of microRNAs had lead to a new era of post-transcriptional regulators of gene expression. Studies from cells, experimental animal models and patients under diabetic conditions demonstrate that expression patterns of microRNAs are altered during the progression of diabetic kidney disease. Functional studies indicate that the ability of microRNAs to bind 3' untranslated region of messenger RNA not only shows their capability to regulate expression of target genes, but also their therapeutic potential to diabetic kidney disease. The presence of microRNAs in plasma, serum, and urine has been shown to be possible biomarkers in diabetic kidney disease. Therefore, identification of the pathogenic role of microRNAs possesses an important clinical impact in terms of prevention and treatment of progression in diabetic kidney disease because it allows us to design novel and specific therapies and diagnostic tools for diabetic kidney disease.
Rong Li; Arthur C K Chung; Xueqing Yu; Hui Y Lan
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Publication Detail:
Type:  Journal Article; Review     Date:  2014-01-14
Journal Detail:
Title:  International journal of endocrinology     Volume:  2014     ISSN:  1687-8337     ISO Abbreviation:  Int J Endocrinol     Publication Date:  2014  
Date Detail:
Created Date:  2014-02-19     Completed Date:  2014-06-24     Revised Date:  2014-06-24    
Medline Journal Info:
Nlm Unique ID:  101516376     Medline TA:  Int J Endocrinol     Country:  Egypt    
Other Details:
Languages:  eng     Pagination:  593956     Citation Subset:  -    
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