A5067949999- Muscle Physiology and Disorders
- Exercise and Physiological Responses
- Tissue Engineering and Regenerative Medicine
- Congenital heart defects research
- Genetic Neurodegenerative Diseases
- Extracellular vesicles in disease
- Cardiac Fibrosis and Remodeling
- Virus-based gene therapy research
- Muscle metabolism and nutrition
- Nerve injury and regeneration
- Heat shock proteins research
- Vitamin D Research Studies
- Silk-based biomaterials and applications
- Galectins and Cancer Biology
- Cardiovascular Disease and Adiposity
- Mitochondrial Function and Pathology
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- MicroRNA in disease regulation
- Cardiomyopathy and Myosin Studies
- Adipose Tissue and Metabolism
- Toxin Mechanisms and Immunotoxins
- Sirtuins and Resveratrol in Medicine
University of Oxford
2016-2023
British Heart Foundation
2020-2021
The University of Melbourne
2015-2019
Abstract Aims After a myocardial infarction, the adult human heart lacks sufficient regenerative capacity to restore lost tissue, leading failure progression. Finding novel ways reprogram cardiomyocytes into state is major therapeutic goal. The epicardium, outermost layer of heart, contributes cardiovascular cell types forming and source trophic signals promote muscle growth during embryonic development. epicardium also essential for regeneration in zebrafish neonatal mice can be reactivated...
During heart development, epicardial cells residing within the outer layer undergo epithelial-mesenchymal transition (EMT) and migrate into underlying myocardium to support organ growth morphogenesis. Disruption of EMT results in embryonic lethality, yet its regulation is poorly understood. Here, we report mesothelial mouse at ultra-high resolution using scanning electron microscopy combined with immunofluorescence analyses. We identified morphologically active regions that associated key...
Duchenne muscular dystrophy (DMD) is an X-linked muscle-wasting disease caused by mutations in the dystrophin gene. DMD boys are wheelchair-bound around 12 years and generally survive into their twenties. There currently no effective treatment except palliative care, although personalized treatments such as exon skipping, stop codon read-through, viral-based gene therapies making progress. Patients present with skeletal muscle pathology, but most also show cardiomyopathy age of 10. A...
Abstract Duchenne muscular dystrophy (DMD) is an X-linked genetic disease characterized by progressive muscle wasting and weakness premature death. Glucocorticoids (e.g. prednisolone) remain the only drugs with a favorable impact on DMD patients, but not without side effects. We have demonstrated that glycine preserves in various models. Since effectively suppresses activity of pro-inflammatory macrophages, we investigated potential treatment to ameliorate dystrophic pathology. Dystrophic...
Duchenne muscular dystrophy (DMD) is a lethal X-linked muscle wasting disorder caused by the absence of dystrophin, large cytoskeletal protein. Increasing levels dystrophin-related-protein utrophin highly promising therapy for DMD and has been shown to improve pathology in dystrophin-deficient mice. One contributing factor mitochondrial that contributes oxidative stress propagates damage. The purpose this study was assess whether could attenuate mitochondria stress. Skeletal muscles from...
Abstract During embryonic heart development, epicardial cells residing within the outer layer of undergo epithelial-mesenchymal transition (EMT) and migrate into myocardium to support stimulate organ growth morphogenesis. Disruption EMT results in aberrant formation lethality. Despite being an essential process during regulation is poorly understood. Here we report on surface at subcellular resolution using scanning electron microscopy (SEM). We identified high- low-EMT regions mesothelial...