Results 21 to 30 of about 491 (128)

The Potentials of Methylene Blue as an Anti-Aging Drug

open access: yesCells, 2021
Methylene blue (MB), as the first fully man-made medicine, has a wide range of clinical applications. Apart from its well-known applications in surgical staining, malaria, and methemoglobinemia, the anti-oxidative properties of MB recently brought new ...
Huijing Xue   +2 more
doaj   +1 more source

Lessons in aging from Myc knockout mouse models

open access: yesFrontiers in Cell and Developmental Biology, 2023
Despite MYC being among the most intensively studied oncogenes, its role in normal development has not been determined as Myc−/− mice do not survival beyond mid-gestation.
Edward V. Prochownik   +4 more
doaj   +1 more source

Implant Supported Prosthesis in a Patient with Progeria: Case Report

open access: yesBiomolecules & Biomedicine, 2009
Prosthodontic rehabilitation can be accomplished with fixed, overdenture, complete, or implant-retained prostheses. Dental treatment overcomes the patient’s functional, psychological, esthetic and phonation problems.
Gözlem Ceylan   +3 more
doaj   +1 more source

Molecular elucidations of hutchinson-gilford progeria syndrome: A hope for managing horrors of premature aging in children

open access: yesPakistan Journal of Pharmaceutical Sciences, 2020
Hutchinson-Gilford progeria syndrome (or Progeria) is an exceptionally rare genetic disorder in children. It is caused by a rare point mutation in the lamin gene. It encodes lamin A protein, resulting in the de-shaping of nuclear membrane.
Bilal Ahmed   +5 more
doaj   +1 more source

Progeria (Hutchinson-Gilford Syndrome): Literature Review and Clinical Case

open access: yesВопросы современной педиатрии, 2022
Progeria, or Hutchinson-Gilford Syndrome is a rare disease from the group of laminopathies characterized by premature aging with skin, bones and cardiovascular system lesions.
Natalia V. Buchinskaya   +3 more
doaj   +1 more source

Increasing the length of progerin's isoprenyl anchor does not worsen bone disease or survival in mice with Hutchinson-Gilford progeria syndrome

open access: yesJournal of Lipid Research, 2009
Hutchinson-Gilford progeria syndrome (HGPS) is caused by the synthesis of a truncated prelamin A, commonly called progerin, that contains a carboxyl-terminal farnesyl lipid anchor.
Brandon S.J. Davies   +10 more
doaj   +1 more source

Chd4 and ThPOK cooperate to preserve structural and electrophysiological integrity of the adult heart through Sprr1a repression

open access: yesThe FEBS Journal, EarlyView.
Chd4/NuRD and ThPOK cooperate to maintain transcriptional repression and nuclear organization in adult cardiomyocytes. Chd4 loss reduces miR‐150‐5p, relieving repression of Sprr1a, while ThPOK loss further enhances Sprr1a activation, possibly through altered chromatin–lamina interactions.
Fadoua El Abdellaoui‐Soussi   +12 more
wiley   +1 more source

Surviving the Nucleus Pulposus Desert: Next‐Generation Strategies for Intervertebral Disc Cell Therapy

open access: yesJOR SPINE, Volume 9, Issue 3, September 2026.
ABSTRACTBackgroundLow back pain remains the leading cause of disability worldwide, with intervertebral disc degeneration representing a major biological contributor. Although cell‐based therapies have shown promise in preclinical models, clinical translation has yielded modest and inconsistent outcomes.
Tynhinane Hamidouche   +9 more
wiley   +1 more source

Activation of the Lactate Receptor GPR81 Ameliorates Senescence Hallmarks and Improves Muscle Function in Cellular and Progeroid Models of Aging

open access: yesAging Cell, Volume 25, Issue 8, August 2026.
Skeletal muscle aging is associated with a decrease in expression of the lactate receptor GPR81. Treating senescent myoblasts in vitro and progeric mice in vivo with GPR81 agonist decreases intramyocellular lipid accumulation and reverses hallmarks of aging. ABSTRACT Skeletal muscle aging is associated with increased lipid accumulation, or myosteatosis,
Pihu Mehrotra   +11 more
wiley   +1 more source

Progerin Hinders Autophagy Flux at Its Final Stages in Hutchinson‐Gilford Progeria Syndrome Cells, Preventing Its Own Autophagic Degradation

open access: yesAging Cell, Volume 25, Issue 8, August 2026.
We demonstrated that progerin induces the formation of autophagosomes but impairs their maturation and subsequent fusion with lysosomes. Progerin impedes proper autophagy flux, thus preventing its own autophagic degradation. Selinexor treatment improved both autophagosome maturation and autophagosome‐lysosome fusion, which ultimately led to effective ...
Ian García‐Aguirre   +18 more
wiley   +1 more source

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