Commentary 10.1172/JCI125616
Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester Medical Center, Rochester, New York, USA.
Address correspondence to: Charles J. Lowenstein, 601 Elmwood Avenue, Box CVRI, Rochester, New York 14624, USA. Phone: 585.276.5077; Email: charles_lowenstein@urmc.rochester.edu.
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Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester Medical Center, Rochester, New York, USA.
Address correspondence to: Charles J. Lowenstein, 601 Elmwood Avenue, Box CVRI, Rochester, New York 14624, USA. Phone: 585.276.5077; Email: charles_lowenstein@urmc.rochester.edu.
Find articles by Bennett, J. in: JCI | PubMed | Google Scholar
First published December 18, 2018 - More info
Hutchinson-Gilford progeria syndrome (HGPS) is a fatal disease characterized by premature aging in which young children fail to thrive and adolescents die from myocardial infarction or stroke. The pathogenesis of HGPS is studied intensively because the mechanisms of premature aging may lead to a better understanding of normal aging. In this issue of the JCI, Osmanagic-Myers and colleagues identify the cellular mechanisms that lead to vascular abnormalities and death in children with HGPS.
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