Key result
Prelamin A accumulation fails to drive atherosclerosis or vascular smooth muscle loss in mice.
Why the study?
Does accumulation of full-length farnesylated prelamin A promote atherosclerosis or vascular smooth muscle loss in a hyperlipidemic mouse model?
Does accumulation of full-length farnesylated prelamin A promote atherosclerosis or vascular smooth muscle loss in a hyperlipidemic mouse model?
In a hyperlipidemic mouse model, accumulation of full-length farnesylated prelamin A does not drive atherosclerosis or vascular smooth muscle cell loss.
BACKGROUND: that lead to expression of an internally truncated, farnesylated prelamin A variant called progerin, which induces loss of vascular smooth muscle cells. Some studies have also reported that accumulation of full-length farnesylated prelamin A, which is normally completely processed to mature nonfarnesylated lamin A, can also drive vascular pathology during physiological aging. METHODS: mice that develop hyperlipidemia on a high-fat diet. RESULTS: mice at 52 weeks of age. There were no differences in proliferation or apoptosis of aortic media cells. CONCLUSIONS: mice.
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Wang et al. (2026) studied Atherosclerosis and vascular smooth muscle loss. Lmna L648R/L648R mutation (Prelamin A accumulation) was evaluated on Proliferation or apoptosis of aortic media cells. Prelamin A accumulation in an Lmna L648R/L648R mouse model does not promote atherosclerosis or vascular smooth muscle loss at 52 weeks of age.
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