Results 71 to 80 of about 21,009 (196)

Resistance training load does not determine resistance training‐induced hypertrophy across upper and lower limbs in healthy young males

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend In healthy young males, we found that skeletal muscle hypertrophy following a period of resistance exercise training (RET) was consistent within and between subjects, as assessed using a variety of established methods. The skeletal muscle hypertrophic response was independent of external load.
Matthew J. Lees   +11 more
wiley   +1 more source

Vascular smooth muscle cell mechanotransduction: Pathways, phenotypes and emerging technologies

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Vascular smooth muscle cells are exposed to mechanical stimuli from the blood flow and the extracellular matrix. The cells sense the signals from cyclic stretch, shear stress, hydrostatic pressure and matrix stiffness through specialized mechanosensors, such as mechanosensitive ion channels or cell surface receptors including ...
Nivethitha Kota Lakshminaraasimulu   +3 more
wiley   +1 more source

The interplay between dynamic regulation of ion‐channel gating and trafficking in cardiac arrhythmogenesis

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Cardiac cellular electrophysiology is modulated by multiple factors, including temperature, extracellular K+, heart rate/pacing frequency, and drugs. These modulators can have distinct effects on ion‐channel gating and transcription/trafficking over time.
Stefan Meier   +3 more
wiley   +1 more source

Duchenne muscular dystrophy treatment with lentiviral vector containing mini‐dystrophin gene in vivo

open access: yesMedComm
Duchenne muscular dystrophy (DMD) is an incurable X‐linked recessive genetic disease caused by mutations in the dystrophin gene. Many researchers aim to restore truncated dystrophin via viral vectors.
Xiaoyu Wang   +11 more
doaj   +1 more source

Dorso‐Ventral and Night‐Day Regulation of Extracellular K+ Dynamics in Mouse Hippocampal Astrocytes

open access: yesGlia, Volume 74, Issue 9, September 2026.
Hippocampal astrocytic K+ buffering varies by region and time. Ventral astrocytes show faster K+ accumulation due to reduced Kir4.1 function. Such regional divergence is modulated by circadian shifts in Kir4.1 and gap junction coupling. ABSTRACT Astrocytes regulate extracellular potassium (K+) through multiple mechanisms operating across distinct ...
Nariman Kiani   +5 more
wiley   +1 more source

Dystrophin and the brain [PDF]

open access: yesDevelopmental Medicine & Child Neurology, 2010
Ricotti, Valeria   +2 more
openaire   +3 more sources

Engineered exosomes improve myocardial cell membrane integrity and heart function in dystrophic cardiomyopathy

open access: yesClinical and Translational Medicine, Volume 16, Issue 8, August 2026.
Schematic diagram of the manufacturing process of exosomes‐cardiac homing peptide (Exo‐CHP) and its therapeutic effects for Duchenne muscular dystrophy (DMD) cardiomyopathy. Abstract Background Duchenne muscular dystrophy (DMD)‐associated cardiomyopathy is a leading causes of premature death, yet treatment options remain limited.
Qihong Wu   +13 more
wiley   +1 more source

Stem cells from umbilical cord blood do have myogenic potential, with and without differentiation induction in vitro

open access: yesJournal of Translational Medicine, 2009
The dystrophin gene, located at Xp21, codifies dystrophin, which is part of a protein complex responsible for the membrane stability of muscle cells. Its absence on muscle causes Duchenne Muscular Dystrophy (DMD), a severe disorder, while a defect of ...
Gollop Thomaz R   +6 more
doaj   +1 more source

Downstream Pathways of Dystrophin Deficiency in Duchenne Muscular Dystrophy: Implications for Muscle Degeneration and Regeneration

open access: yesJournal of Cachexia, Sarcopenia and Muscle, Volume 17, Issue 4, August 2026.
ABSTRACT Background Duchenne muscular dystrophy (DMD) is the most common and severe form of muscular dystrophy, primarily affecting skeletal muscle and leading to premature death. Although the loss of dystrophin has long been recognised as the primary cause of the disease, no definitive cure is currently available. As a consequence, therapeutic efforts
Raffaele Epis   +5 more
wiley   +1 more source

Shorter Phosphorodiamidate Morpholino Splice-Switching Oligonucleotides May Increase Exon-Skipping Efficacy in DMD

open access: yesMolecular Therapy: Nucleic Acids, 2018
Duchenne muscular dystrophy is a fatal muscle disease, caused by mutations in DMD, leading to loss of dystrophin expression. Phosphorodiamidate morpholino splice-switching oligonucleotides (PMO-SSOs) have been used to elicit the restoration of a ...
Ugur Akpulat   +6 more
doaj   +1 more source

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