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suck abstract from ncbi


10.3390/genes9020098

http://scihub22266oqcxt.onion/10.3390/genes9020098
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C5852594!5852594!29462869
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suck abstract from ncbi


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pmid29462869      Genes+(Basel) 2018 ; 9 (2): ä
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  • Modulation of VEGF-A Alternative Splicing as a Novel Treatment in Chronic Kidney Disease #MMPMID29462869
  • Stevens M; Oltean S
  • Genes (Basel) 2018[Feb]; 9 (2): ä PMID29462869show ga
  • Vascular endothelial growth factor A (VEGF-A) is a prominent pro-angiogenic and pro-permeability factor in the kidney. Alternative splicing of the terminal exon of VEGF-A through the use of an alternative 3? splice site gives rise to a functionally different family of isoforms, termed VEGF-Axxxb, known to have anti-angiogenic and anti-permeability properties. Dysregulation of the VEGF-Axxx/VEGF-Axxxb isoform balance has recently been reported in several kidney pathologies, including diabetic nephropathy (DN) and Denys?Drash syndrome. Using mouse models of kidney disease where the VEGF-A isoform balance is disrupted, several reports have shown that VEGF-A165b treatment/over-expression in the kidney is therapeutically beneficial. Furthermore, inhibition of certain splice factor kinases involved in the regulation of VEGF-A terminal exon splicing has provided some mechanistic insight into how VEGF-A splicing could be regulated in the kidney. This review highlights the importance of further investigation into the novel area of VEGF-A splicing in chronic kidney disease pathogenesis and how future studies may allow for the development of splicing-modifying therapeutic drugs.
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