Hutchinson-Gilford progeria syndrome, cardiovascular disease and oxidative stress

摘要: Hutchinson-Gilford Progeria Syndrome (HGPS), a rare human disease characterized by premature aging, is mainly caused the abnormal accumulation of progerin, mutant form mammalian nuclear envelope component lamin A. HGPS patients exhibit vascular alterations and die at an average age 13 years, predominantly from myocardial infarction or stroke. Animal models have been valuable tool in study pathological processes implicated origin this its associated cardiovascular alterations. Some molecular mechanisms might be relevant to process normal since progerin detected cells elderly humans. Conversely, linked such as increase oxidative stress, pathogenic HGPS. In review, we discuss recent advances understanding underlying with HGPS, potential role therapeutic approaches for treatment devastating disease.