Journal
GENES
Volume 9, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/genes9020098
Keywords
VEGF-A; alternative splicing; kidney disease
Categories
Funding
- British Heart Foundation [PG/15/53/31371]
- Diabetes UK [17/000568]
- Richard Bright VEGF Research Trust
- BBSRC [BB/J007293/2, BB/P012035/1, BB/J007293/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/P012035/1, BB/J007293/2, BB/J007293/1] Funding Source: researchfish
- British Heart Foundation [PG/15/53/31371] Funding Source: researchfish
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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-A(xxx)b, known to have anti-angiogenic and anti-permeability properties. Dysregulation of the VEGF-A(xxx)/VEGF-A(xxx)b 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-A(165)b 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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