Results 81 to 90 of about 18,188 (219)

Targeting a therapeutic LIF transgene to muscle via the immune system ameliorates muscular dystrophy. [PDF]

open access: yes, 2019
Many potentially therapeutic molecules have been identified for treating Duchenne muscular dystrophy. However, targeting those molecules only to sites of active pathology is an obstacle to their clinical use.
Bertoni, Carmen   +6 more
core  

Senolytics and exercise: Dual modalities for rejuvenating muscle

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend The role of senolytics on the heart and skeletal muscle. Senescent cell burden increases with ageing, disuse and disease. The senolytics dasatinib+quercetin (D+Q), navitoclax and fisetin, as well as exercise, eliminate senescent cells, reducing senescent cell burden and their senescence‐associated secretory phenotype (SASP ...
Zeynep Elif Yesilyurt‐Dirican   +4 more
wiley   +1 more source

Functional rescue of dystrophin deficiency in mice caused by frameshift mutations using Campylobacter jejuni Cas9 [PDF]

open access: yes, 2018
Duchenne muscular dystrophy (DMD) is a fatal, X-linked muscle wasting disease caused by mutations in the DMD gene. In 51% of DMD cases, a reading frame is disrupted because of deletion of several exons.
Cappellari, O   +9 more
core   +2 more sources

The mitochondrial‐targeted antioxidant SkQ1 prevents skeletal muscle mitochondrial‐apoptotic but not necroptotic signalling during ovarian cancer

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend An evaluation of the degree to which mitochondrial hydrogen peroxide emission (mH2O2)‐mediated apoptotic and necroptotic signalling contributes to skeletal muscle atrophy in an orthotopic epithelial ovarian cancer (EOC) model. To determine whether attenuating mH2O2 could prevent regulated cell death signalling and mitigate muscle
Shahrzad Khajehzadehshoushtar   +15 more
wiley   +1 more source

Caspase-12 ablation preserves muscle function in the mdx mouse [PDF]

open access: yesHuman Molecular Genetics, 2014
Duchenne muscular dystrophy (DMD) is a devastating muscle wasting disease caused by mutations in dystrophin. Several downstream consequences of dystrophin deficiency are triggers of endoplasmic reticulum (ER) stress, including loss of calcium homeostasis, hypoxia and oxidative stress.
Catherine, Moorwood, Elisabeth R, Barton
openaire   +2 more sources

Measuring neuromuscular junction functionality [PDF]

open access: yes, 2017
Neuromuscular junction (NMJ) functionality plays a pivotal role when studying diseases in which the communication between motor neuron and muscle is impaired, such as aging and amyotrophic lateral sclerosis (ALS).
Del Prete, Zaccaria   +4 more
core   +1 more source

The Age‐Dependent Resident Myonuclear Multi‐Omic Response to an Acute Skeletal Muscle Hypertrophic Stimulus in Mice

open access: yesAdvanced Science, Volume 13, Issue 25, 4 May 2026.
Resident myonuclei are the molecular “control centers” for large multinuclear muscle fibers. It is presumed that, with aging, these control centers become compromised and contribute to delayed or blunted muscle adaptive potential. This study is a detailed roadmap that exposes how young versus aged myonuclei respond to a hypertrophic loading stimulus ...
Pieter J. Koopmans   +8 more
wiley   +1 more source

Histological Study of Masseter Muscle in a Mouse Muscular Dystrophy Model (mdx mouse).

open access: yesThe Bulletin of Tokyo Dental College, 2000
Histological changes in the masseter muscle were observed over time in mdx mice, a muscular dystrophy model. It was found that marked necrosis occurs about the time of weaning at around 4 weeks of age; then the tissue actively regenerates at 8 weeks and stabilizes as regenerated muscle with centronuclei at 15 weeks old.
S, Abe   +5 more
openaire   +3 more sources

Revertant fibres and dystrophin traces in Duchenne muscular dystrophy: Implication for clinical trials [PDF]

open access: yes, 2010
Duchenne muscular dystrophy (DMD) is characterised by the absence of dystrophin in muscle biopsies, although residual dystrophin can be present, either as dystrophin-positive (revertant) fibres or traces.
Arechavala-Gomeza, V   +12 more
core   +1 more source

Patient‐Derived 3D Bioprinted Cardiac Organoid Constructs Reveal Key Pathological Features of Duchenne Muscular Dystrophy

open access: yesAdvanced Healthcare Materials, Volume 15, Issue 16, 24 April 2026.
Patient‐derived cardiac organoids reveal key features of Duchenne muscular dystrophy cardiomyopathy, including apoptosis, oxidative stress, calcium handling defects, and mechanical remodeling. By integrating organoids into alginate–gelatin bioprinted constructs, disease phenotypes are organized into scalable 3D cardiac tissues displaying extracellular ...
Vittoria Marini   +15 more
wiley   +1 more source

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