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Harnessing the Power of SIRT1 and Non-coding RNAs in Vascular Disease

Journal

CURRENT NEUROVASCULAR RESEARCH
Volume 14, Issue 1, Pages 82-88

Publisher

BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1567202613666161129112822

Keywords

Aging; apoptosis; autophagy; biomarker; cardiovascular disease; CCN4; cyclin-dependent kinase 2 (CDK2); cyclin-dependent kinase inhibitor 1 (p21); cell cycle; circular RNA; diabetes mellitus; endothelial cells; forkhead transcription factors; FoxO; metabolism; microRNA; non-coding RNA; oxidative stress; programmed cell death; senescence; SIRT1; stem cells; transcription factors; WISP1; Wnt signaling

Funding

  1. American Diabetes Association
  2. American Heart Association
  3. NIH NIEHS
  4. NIH NIA
  5. NIH NINDS
  6. NIH ARRA

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Noncommunicable diseases (NCDs) contribute to a significant amount of disability and death in the world. Of these disorders, vascular disease is ranked high, falls within the five leading causes of death, and impacts multiple other disease entities such as those of the cardiac system, nervous system, and metabolic disease. Targeting the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1) pathway and the modulation of micro ribonucleic acids (miRNAs) may hold great promise for the development of novel strategies for the treatment of vascular disease since each of these pathways are highly relevant to cardiac and nervous system disorders as well as to metabolic dysfunction. SIRT1 is vital in determining the course of stem cell development and the survival, metabolism, and life span of differentiated cells that are overseen by both autophagy and apoptosis. SIRT1 interfaces with a number of pathways that involve forkhead transcription factors, mechanistic of rapamycin (mTOR), AMP activated protein kinase (AMPK) and Wnt1 inducible signaling pathway protein 1 (WISP1) such that the level of activity of SIRT1 can become a critical determinant for biological and clinical outcomes. The essential fine control of SIRT1 is directly tied to the world of non-coding RNAs that ultimately oversee SIRT1 activity to either extend or end cellular survival. Future studies that can further elucidate the crosstalk between SIRT1 and non-coding RNAs should serve well our ability to harness the power of SIRT1 and non-coding RNAs for the treatment of vascular disorders.

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