Results 71 to 80 of about 7,451 (172)

Hematopoietic (stem) cells—The elixir of life?

open access: yesFEBS Letters, Volume 600, Issue 4, Page 392-417, February 2026.
The aging of HSCs (hematopoietic stem cells) and the blood system leads to the decline of other organs. Rejuvenating aged HSCs improves the function of the blood system, slowing the aging of the heart, kidney, brain, and liver, and the occurrence of age‐related diseases.
Emilie L. Cerezo   +4 more
wiley   +1 more source

Posttranslational Modifications of Lamin A/C and Cardiac Aging: A Short Review

open access: yesJournal of the Practice of Cardiovascular Sciences
Cardiac aging is considered as natural and age-related changes in the heart, which can lead to a decline in heart function. Cardiac aging increases the risk of heart failure, atrial fibrillation, and other cardiovascular complications.
Vikas Tiwari   +2 more
doaj   +1 more source

Management of cataract in Werner syndrome

open access: yesIndian Journal of Ophthalmology, 2018
Werner syndrome (WS) is a rare progressive disorder. It is characterized by the appearance of unusually accelerated aging (progeria) including bilateral senile cataract. Here, we report a successful management of hypermature cataract in WS.
Rakhi Kusumesh   +3 more
doaj   +1 more source

A Cell-Intrinsic Interferon-like Response Links Replication Stress to Cellular Aging Caused by Progerin

open access: yesCell Reports, 2018
Summary: Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disease caused by a truncated lamin A protein (progerin) that drives cellular and organismal decline.
Ray Kreienkamp   +9 more
doaj   +1 more source

Current advances and future prospects of cell reprogramming in progeroid syndromes

open access: yesFrontiers in Cell and Developmental Biology
Cell reprogramming consists in the reverse process to cell differentiation, making cells lose their identity and age-related characteristics and granting an increased potential for proliferation and redifferentiation on different lineages.
Lucas Moledo-Nodar   +6 more
doaj   +1 more source

Mutation in Genes FBN1, AKT1, and LMNA: Marfan Syndrome, Proteus Syndrome, and Progeria Share Common Systemic Involvement

open access: yesInternational Journal of Medical Students, 2015
Genetic mutations are becoming more deleterious day by day. Mutations of Genes named FBN1, AKT1, LMNA result specific protein malfunction that in turn commonly cause Marfan syndrome, Proteus syndrome, and Progeria, respectively.
Tonmoy Biswas
doaj   +1 more source

Progeria

open access: yesRevista chilena de pediatría, 2002
Resumen La progeria o síndrome de Hutchinson-Gilford esun síndrome poco frecuente. Consiste en la aparición de signos de envejecimiento en niños entre su primer y segundo año de vida. La mayoría de los casos de progeria son esporádicos, lo cual plantea la posibilidad de un patrón de herencia autosómico dominante por mutación de novo.
Pardo V., Rosa Andrea   +1 more
openaire   +2 more sources

Progerin accelerates atherosclerosis by inducing endoplasmic reticulum stress in vascular smooth muscle cells

open access: yesEMBO Molecular Medicine, 2019
Hutchinson–Gilford progeria syndrome (HGPS) is a rare genetic disorder caused by progerin, a mutant lamin A variant. HGPS patients display accelerated aging and die prematurely, typically from atherosclerosis complications. Recently, we demonstrated that
Magda R Hamczyk   +9 more
doaj   +1 more source

Progeria and Atherosclerosis [PDF]

open access: yesArchives of Disease in Childhood, 1955
A J, KEAY, M F, OLIVER, G S, BOYD
openaire   +2 more sources

Hutchinson-Gilford Progeria as a Window into Human Aging: Genetic, Cellular, and Therapeutic Perspectives

open access: yesMedicina U.P.B.
Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare and devastating genetic disorder characterized by premature aging. This condition is caused by an autosomal dominant mutation in the LMNA gene, which leads to the production of the defective protein ...
María Elena Arana Baquero   +2 more
doaj   +1 more source

Home - About - Disclaimer - Privacy