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oai:repisalud.isciii.es:20.500.12105/79592024-09-27T08:23:11Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Dorado, Beatriz author Andres, Vicente author 2017 Lamin A is a nuclear intermediate filament protein with important structural and regulatory roles in most differentiated mammalian cells. Excessive accumulation of its precursor prelamin A or the mutant form called 'progerin' causes premature aging syndromes. Progeroid 'laminopathies' are characterized by severe cardiovascular problems (cardiac electrical defects, vascular calcification and stiffening, atherosclerosis, myocardial infarction, and stroke) and premature death. Here, we review studies in cell and mouse models and patients that are unraveling how abnormal prelamin A and progerin accumulation accelerates cardiovascular disease and aging. This knowledge is essential for developing effective therapies to treat progeria and may help identify new mechanisms underlying normal aging. Curr Opin Cell Biol. 2017; 46:17-25 10.1016/j.ceb.2016.12.005 1879-0410 0955-0674 Current opinion in cell biology 28086161 http://hdl.handle.net/20.500.12105/7959 A-type lamins and cardiovascular disease in premature aging syndromes