Lamin A/C Expression in Hematopoietic Cells Declines During Human Aging and Constrains Atherosclerosis in Mice.
Abstract
Aging is the primary risk factor for atherosclerosis, a degenerative process regulated by immune cells and the leading cause of death worldwide. Previous studies on premature aging syndromes have linked atherosclerosis to defects in A-type lamins, key nuclear envelope components. However, whether these defects influence atherosclerosis during normal aging remains unexplored. Here, we examined how aging affects lamin A/C expression in circulating leukocytes and investigated the impact of manipulating their expression in hematopoietic cells on their function and atherosclerosis progression.
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Research summary
The paper claims that the decline of lamin A/C expression in hematopoietic cells during aging contributes to atherosclerosis progression. This research is relevant as it explores a potential mechanism linking aging to atherosclerosis, addressing a root cause of age-related diseases rather than merely treating symptoms.
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