Results 71 to 80 of about 3,816 (187)

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

, 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, Adams, David J, Atkinson, James, Balmus, Gabriel, Barros, Ana C, Clift, Dean, Collins, Casey, Demir, Mukerrem, Geisler, Nicola J, Jackson, Stephen P, Jacobsen, Matt, Karp, Natasha A, Kirton, Andrea, Larrieu, Delphine, Lelliott, Christopher J, Rodriguez, Raphael, Sanger Mouse Genetics Project, White, Jacqueline K   +17 more
core   +2 more sources

Research Models for Studying Vascular Calcification [PDF]

, 2020
Calcification of the vessel wall contributes to high cardiovascular morbidity and mortality. Vascular calcification (VC) is a systemic disease with multifaceted contributing and inhibiting factors in an actively regulated process.
Babic, Milen, Giet, Markus van der, Herrmann, Jaqueline, Schuchardt, Mirjam, Tölle, Markus   +4 more
core   +1 more source

Proteostasis of organelles in aging and disease

The 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, Cansu Doğan, Dunja Petrović, Gülce Perçin, Seda Koyuncu, David Vilchez   +5 more
wiley   +1 more source

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

, 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, Dal Sasso, Eleonora, Forte, Maurizio, Frati, Giacomo, Gerosa, Gino, Iop, Laura, Palmerio, Silvia, Peruzzi, Mariangela, Schirone, Leonardo, Sciarretta, Sebastiano   +9 more
core   +4 more sources

Hematopoietic (stem) cells—The elixir of life?

FEBS 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, Jonah Anderson, Emilie Dinh Vedrenne, Noël Yeh Martín, Jette Lengefeld   +4 more
wiley   +1 more source

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

Clinical, 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, Ciążyńska M, Kabziński J, Majsterek I, Sobolewska-Sztychny D, Narbutt J, Lesiak A   +6 more
doaj  

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

Frontiers 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, Lyudmila I. Kutueva, Svetlana Y. Kurchashova, Igor I. Kireev   +3 more
doaj   +1 more source

Personalized Models of Biological Barriers and Their Diseases: Recent Progress with Organs‐On‐Chips

Advanced Biology, Volume 10, Issue 2, February 2026.
Buck and Bugter et al. explore the architectural diversity and physiological functions of human barrier systems and reveal how organ‐on‐chip platforms, particularly those integrating patient‐derived cells, are advancing barrier disease modeling. They highlight how emerging biological and technological advances can be used to bridge the gap between ...
Franziska Buck, Jeroen Bugter, Gizem Yorukoglu, Mina Kazemzadeh Dastjerd, Thomas E. Winkler   +4 more
wiley   +1 more source

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

European 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, C. Capanni, M. Columbaro, M. Ortolani, M.R. D'Apice, G. Novelli, M. Fini, S. Marmiroli, E. Scarano, N.M. Maraldi, S. Squarzoni, S. Prencipe, G. Lattanzi   +12 more
doaj   +1 more source

Nuclear envelope budding inhibition slows down progerin-induced aging process. [PDF]

Proc Natl Acad Sci U S A
Progerin causes Hutchinson–Gilford progeria syndrome (HGPS), but how progerin accelerates aging is still an interesting question. Here, we provide evidence linking nuclear envelope (NE) budding and accelerated aging. Mechanistically, progerin disrupts nuclear lamina to induce NE budding in concert with lamin A/C, resulting in transport of chromatin ...
Wang X, Ma L, Lu D, Zhao G, Ren H, Lin Q, Jia M, Huang F, Wang S, Xu Z, Yang Z, Chu Y, Xu Z, Li W, Yu L, Jiang Q, Zhang C.   +16 more
europepmc   +3 more sources