Results 91 to 100 of about 3,871 (195)

Potential Benefits of Allogeneic Haploidentical Adipose Tissue-Derived Stromal Vascular Fraction in a Hutchinson–Gilford Progeria Syndrome Patient

open access: yesFrontiers in Bioengineering and Biotechnology, 2020
Hutchinson–Gilford progeria syndrome (HGPS) is a rare, fatal, and genetic disorder in the LMNA gene encoding for prelamin A. Normally, prelamin A is processed to become lamin A protein.
Jaewoo Pak   +7 more
doaj   +1 more source

From Cellular Characteristics to Disease Diagnosis: Uncovering Phenotypes with Supercells [PDF]

open access: yes, 2013
Cell heterogeneity and the inherent complexity due to the interplay of multiple molecular processes within the cell pose difficult challenges for current single-cell biology.
Banavar, Jayanth R.   +12 more
core   +5 more sources

Ignoring the planet: A critical blind spot for research on ageing

open access: yesJournal of Internal Medicine, Volume 298, Issue 6, Page 578-590, December 2025.
Abstract Although research on ageing has largely concentrated on understanding the fundamental biology of the ageing process and devising pharmaceutical interventions in order to slow it down, increasing evidence has underscored the crucial role of environmental inputs across the life course and across generations, in shaping both individual and ...
Paul Shiels   +6 more
wiley   +1 more source

New therapeutic approaches to HGPS based on progerin inhibition [PDF]

open access: yesOrphanet Journal of Rare Diseases, 2015
Hutchinson-Gilford Progeria Syndrome (HGPS) is caused by a de novo heterozygous mutation on LMNA gene that leads to accumulation of progerin, a mutant form of prelamin A. HGPS skin fibroblasts are characterized by multiple nuclear defects: nuclear shape abnormalities chromatin structure alterations, increased DNA damage and cell cycle alterations ...
openaire   +1 more source

Mouse models of ageing and their relevance to disease [PDF]

open access: yes, 2016
Ageing is a process that gradually increases the organism’s vulnerability to death. It affects different biological pathways, and the underlying cellular mechanisms are complex.
Dogan, Soner   +5 more
core   +2 more sources

Decoding Dental Stem Cell Aging: Mechanisms, Therapeutic Strategies, and Beyond

open access: yesAdvanced Science, Volume 12, Issue 44, November 27, 2025.
Dental stem cell (DSC) aging involves genomic instability, mitochondrial dysfunction, telomere attrition, and epigenetic alterations, leading to impaired proliferation, reduced differentiation potential, and pro‐inflammatory secretory activity. These processes drive cellular senescence and compromise regenerative and immunomodulatory functions, thereby
Xinyuan Zhao   +7 more
wiley   +1 more source

New insights into applications of base editor in hereditary disorders

open access: yesInterdisciplinary Medicine, Volume 3, Issue 6, November 2025.
Abstract Hereditary disorders are a group of diseases caused by genetic mutations or chromosomal variations. Although the incidence of each genetic disorder is relatively low, patients affected by the disease generally experience a range of severe symptoms, including blindness, disability, and even premature death. In addition, the available treatments
Maoping Cai   +8 more
wiley   +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

Potential Role of p53 in Huchinson-Gilford Progeria Syndrome [PDF]

open access: yes, 2017
Undergraduate ...
Eschedor, Danielle   +2 more
core  

Barrier-to-autointegration factor 1 protects against a basal cGAS-STING response [PDF]

open access: yes, 2020
Although the pathogen recognition receptor pathways that activate cell-intrinsic antiviral responses are well delineated, less is known about how the host regulates this response to prevent sustained signaling and possible immune-mediated damage. Using a
Artyomov, Maxim   +11 more
core   +2 more sources

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