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Emerging role of HuR in inflammatory response in kidney diseases
1Nephrology Hospital, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Human antigen R (HuR) is a member of the embryonic lethal abnormal vision (ELAV) family which can bind to the A/U rich elements in 3' un-translated region of mRNA and regulate mRNA splicing, transportation, and stability. Unlike other members of the ELAV family, HuR is ubiquitously expressed. Early studies mainly focused on HuR function in malignant diseases. As researches proceed, more and more proofs demonstrate its relationship with inflammation. Since most kidney diseases involve pathological changes of inflammation, HuR is now suggested to play a pivotal role in glomerular nephropathy, tubular ischemia-reperfusion damage, renal fibrosis and even renal tumors. By regulating the mRNAs of target genes, HuR is causally linked to the onset and progression of kidney diseases. Reports on this topic are steadily increasing, however, the detailed function and mechanism of action of HuR are still not well understood. The aim of this review article is to summarize the present understanding of the role of HuR in inflammation in kidney diseases, and we anticipate that future research will ultimately elucidate the therapeutic value of this novel target.
Human antigen R (HuR) is a member of the embryonic lethal abnormal vision (ELAV) family which can bind to the A/U rich elements in 3' un-translated region of mRNA and regulate mRNA splicing, transportation, and stability. Unlike other members of the ELAV family, HuR is ubiquitously expressed. Early studies mainly focused on HuR function in malignant diseases. As researches proceed, more and more proofs demonstrate its relationship with inflammation. Since most kidney diseases involve pathological changes of inflammation, HuR is now suggested to play a pivotal role in glomerular nephropathy, tubular ischemia-reperfusion damage, renal fibrosis and even renal tumors. By regulating the mRNAs of target genes, HuR is causally linked to the onset and progression of kidney diseases. Reports on this topic are steadily increasing, however, the detailed function and mechanism of action of HuR are still not well understood. The aim of this review article is to summarize the present understanding of the role of HuR in inflammation in kidney diseases, and we anticipate that future research will ultimately elucidate the therapeutic value of this novel target.
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