Sirtuin 2 deficiency aggravates ageing-induced vascular remodelling in humans and mice
Authors' conclusion
The deacetylase SIRT2 is a response to ageing that delays vascular ageing, and the cytoplasm-mitochondria axis (SIRT2-p66Shc-mROS) is important for vascular ageing.
Study context
- Population
- Human and mouse aortas; young and old wild-type and Sirt2 knockout mice
- Comparison
- Sirt2 knockout vs wild-type mice, young and old
Main finding
As reported in the abstract
- Among sirtuins, SIRT2 had the highest levels in human and mouse aortas
- SIRT2 activity reduced in aged aortas; loss of SIRT2 accelerated vascular ageing
- In old mice, SIRT2 deficiency aggravated ageing-induced arterial stiffness and constriction-relaxation dysfunction, with aortic remodelling (thickened medial layers, elastin fibre breakage, collagen deposition, inflammation)
- p66Shc and mitochondrial ROS (mROS) metabolism contributed to SIRT2 function in vascular ageing
- SIRT2 repressed p66Shc activation and mROS production by deacetylating p66Shc at lysine 81
- ROS elimination by MnTBAP repressed SIRT2 deficiency-mediated aggravation of vascular remodelling and dysfunction in angiotensin II-challenged and aged mice
- SIRT2 coexpression module in aortas reduced with ageing across species; significant predictor of age-related aortic diseases in humans
Original publication
Sirtuin 2 deficiency aggravates ageing-induced vascular remodelling in humans and mice. Eur Heart J. Published 28 June 2023. doi:10.
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