Progeria and accelerated cardiovascular aging

Molecular and Cellular Mechanisms Contributing to the Accelerated Aging Phenotype in Hutchinson-gilford Progeria Syndrome

Progeria, rapamycin and normal aging: recent breakthrough

A recent discovery that rapamycin suppresses a pro-senescent phenotype in progeric cells not only suggests a non-toxic therapy for progeria but also implies its similarity with normal aging. For one, rapamycin is also known to suppress aging of regular human cells. Here I discuss four potential scenarios, comparing progeria with both normal and accelerated aging. This reveals further indication...

Aging: Progeria and the Lamin Connection

The relationship between progerias--diseases that resemble premature aging--and the normal aging process has been a source of debate in the aging research community. A recent study finds that LMNA, a gene targeted for mutation in Hutchinson Gilford Progeria Syndrome, may control the onset of aging-associated decline in normal fibroblasts.

Progeria: a cell culture study on aging.

Progeria is an autosomal recessive disorder showing precocious senility. The cultured skin fibroblast from both the homozygous affected individual and the heterozygous parents can be distinguished from normals by decreased cell growth in culture. Mitotic activity, DNA synthesis, and cloning efficiency are markedly reduced.

Cardiovascular pathology in Hutchinson-Gilford progeria: correlation with the vascular pathology of aging.

OBJECTIVE Children with Hutchinson-Gilford progeria syndrome (HGPS) exhibit dramatically accelerated cardiovascular disease (CVD), causing death from myocardial infarction or stroke between the ages of 7 and 20 years. We undertook the first histological comparative evaluation between genetically confirmed HGPS and the CVD of aging. METHODS AND RESULTS We present structural and immunohistologi...