Endothelial-to-Mesenchymal Transition Contributes to Accelerated Atherosclerosis in Hutchinson-Gilford Progeria Syndrome.

Magda R Hamczyk, Rosa M Nevado, Pilar Gonzalo, María J Andrés-Manzano, Paula Nogales, Víctor Quesada, Aránzazu Rosado, Carlos Torroja, Fátima Sánchez-Cabo, Ana Dopazo, Jacob F Bentzon, Carlos López-Otín, Vicente Andrés

Departamento de Bioquímica y Biología Molecular, Instituto Universitario de Oncología, Universidad de Oviedo, Spain (M.R.H., V.Q., C.L.-O.).Departamento de Bioquímica y Biología Molecular, Instituto Universitario de Oncología, Universidad de Oviedo, Spain (M.R.H., V.Q., C.L.-O.). · pubmed

Paper

Abstract

Atherosclerosis is the main medical problem in Hutchinson-Gilford progeria syndrome, a rare premature aging disorder caused by the mutant lamin-A protein progerin. Recently, we found that limiting progerin expression to vascular smooth muscle cells (VSMCs) is sufficient to hasten atherosclerosis and death in

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Research summary

The paper addresses the role of endothelial-to-mesenchymal transition in the context of Hutchinson-Gilford progeria syndrome, which is a model for studying accelerated aging and its associated vascular complications. While it contributes to understanding the mechanisms underlying atherosclerosis in a premature aging disorder, the findings primarily focus on a specific disease rather than addressing broader root causes of aging or lifespan extension. Thus, it represents solid research but with limited impact on the overall field of longevity research.

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