Results 71 to 80 of about 3,871 (195)

First Generation Proteolysis Targeting Chimeras (PROTACs) for the Treatment of Progeria

open access: yesAdvanced Science, EarlyView.
We report the first PROTACs designed to degrade progerin, introducing a novel therapeutic approach for progeria. The best compound, UCM‐18142, significantly reduces progerin levels and improves key disease phenotypes in patient‐derived cells and in the LmnaG609G/G609G mouse model, paving the way for new treatment strategies targeting the root cause of ...
Jon Macicior‐Michelena   +5 more
wiley   +1 more source

Targeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome. [PDF]

open access: yes, 2018
Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare, but devastating genetic disease characterized by segmental premature aging, with cardiovascular disease being the main cause of death.
Abrudan, Monica   +17 more
core   +2 more sources

Proteostasis of organelles in aging and disease

open access: yesThe FEBS Journal, EarlyView.
Cells rely on regulated proteostasis mechanisms to keep their internal compartments functioning properly. When these mechanisms fail, damaged proteins accumulate, disrupting organelles, such as the nucleus, mitochondria, endoplasmic reticulum, Golgi, and lysosomes, as well as membraneless organelles, such as stress granules, processing bodies, the ...
Yara Nabawi   +5 more
wiley   +1 more source

More Than Skin Deep – the Effects of Ultraviolet Radiation on Cathepsin K and Progerin Expression in Cultured Dermal Fibroblasts

open access: yesClinical, Cosmetic and Investigational Dermatology, 2021
Igor Aleksander Bednarski,1 Magdalena Ciążyńska,2 Jacek Kabziński,3 Ireneusz Majsterek,3 Dorota Sobolewska-Sztychny,1 Joanna Narbutt,1 Aleksandra Lesiak1 1Department of Dermatology, Pediatric Dermatology and Dermatological ...
Bednarski IA   +6 more
doaj  

The light and shadow of senescence and inflammation in cardiovascular pathology and regenerative medicine [PDF]

open access: yes, 2017
Recent epidemiologic studies evidence a dramatic increase of cardiovascular diseases, especially associated with the aging of the world population. During aging, the progressive impairment of the cardiovascular functions results from the compromised ...
Cavarretta, Elena   +9 more
core   +4 more sources

Advances in CRISPR Base Editing: From Molecular Evolution to Therapeutic Applications in Genomic Medicine

open access: yesJournal of Cellular and Molecular Medicine, Volume 30, Issue 8, April 2026.
ABSTRACT CRISPR‐Cas9 systems revolutionized gene editing, but inherent drawbacks, namely DNA double‐strand breaks (DSBs) and the difficulty of achieving precise repairs (due to low HDR efficiency), led researchers to invent new, more accurate gene editing tools.
Melike Aliciaslan   +3 more
wiley   +1 more source

Are There Common Mechanisms Between the Hutchinson–Gilford Progeria Syndrome and Natural Aging?

open access: yesFrontiers in Genetics, 2019
The Hutchinson–Gilford progeria syndrome (HGPS) is a premature aging disease caused by mutations of the LMNA gene leading to increased production of a partially processed form of the nuclear fibrillar protein lamin A – progerin.
Vasily V. Ashapkin   +3 more
doaj   +1 more source

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

Recent Advances in Animal and Human Pluripotent Stem Cell Modeling of Cardiac Laminopathy [PDF]

open access: yes, 2016
published_or_final_versio
Jiang, Y   +7 more
core   +1 more source

Autophagic degradation of farnesylated prelamin A as a therapeutic approach to lamin-linked progeria

open access: yesEuropean Journal of Histochemistry, 2011
Farnesylated prelamin A is a processing intermediate produced in the lamin A maturation pathway. Accumulation of a truncated farnesylated prelamin A form, called progerin, is a hallmark of the severe premature ageing syndrome, Hutchinson-Gilford progeria.
V. Cenni   +12 more
doaj   +1 more source

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