Alternative Splicing: A Key Mediator of Diabetic Vasculopathy

Victoria A. Cornelius, Jenna R. Fulton, Andriana Margariti*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

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Abstract

Cardiovascular disease is the leading cause of death amongst diabetic individuals. Atherosclerosis is the prominent driver of diabetic vascular complications, which is triggered by the detrimental effects of hyperglycemia and oxidative stress on the vasculature. Research has extensively shown diabetes to result in the malfunction of the endothelium, the main component of blood vessels, causing severe vascular complications. The pathogenic mechanism in which diabetes induces vascular dysfunction, however, remains largely unclear. Alternative splicing of protein coding pre-mRNAs is an essential regulatory mechanism of gene expression and is accepted to be intertwined with cellular physiology. Recently, a role for alternative splicing has arisen within vascular health, with aberrant mis-splicing having a critical role in disease development, including in atherosclerosis. This review focuses on the current knowledge of alternative splicing and the roles of alternatively spliced isoforms within the vasculature, with a particular focus on disease states. Furthermore, we explore the recent elucidation of the alternatively spliced QKI gene within vascular cell physiology and the onset of diabetic vasculopathy. Potential therapeutic strategies to restore aberrant splicing are also discussed.
Original languageEnglish
Pages (from-to)e1332
JournalGenes
Volume12
Issue number9
Early online date27 Aug 2021
DOIs
Publication statusEarly online date - 27 Aug 2021

Keywords

  • alternative splicing
  • cardiovascular disease
  • diabetic vasculopathy
  • atherosclerosis
  • isoforms
  • quaking
  • QKI
  • therapeutic strategies

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