CP
Publications
- Myostatin deletion reverses myosteatosis and improves angiogenesis in obese mice
- Metabolic regulation of endothelial reactive oxygen species production in obesity
- The biological clock enhancer nobiletin ameliorates steatosis in obesity by restoring aberrant hepatic circadian rhythm.
- Loss of GTPase activating protein neurofibromin stimulates paracrine cell communication via macropinocytosis
- Obesity Induces Disruption of Microvascular Endothelial Circadian Rhythm
- Early Endothelial Dysfunction in a Novel Model of Sustained Hyperphagia and Obesity in Mice Using a Brain Targeting Adeno-Associated Virus
- Mechanisms of Myosteatosis in Obesity and the Effects of Muscle Hypertrophy
- Increased Muscle Mass Restores a Healthy Vascular Endothelial Cell Phenotype in Obesity
- Galectin‐3 Regulates Oxidant Stress in Obesity
- Deletion of Myostatin Resolves Myosteatosis and Improves Angiogenesis in Obese Mice
- Generation of an Adeno‐Associated Viral Model of Murine Obesity
- PFKFB3 Mediated Changes in ROS/NO Balance Contribute to Endothelial Dysfunction in Obesity
- Novel roles of PFKFB3 in mediating endothelial dysfunction in obesity
- Galectin-3 Mediates Vascular Dysfunction in Obesity by Regulating NADPH Oxidase 1
- Tissue Clearing: An Overview of Methods, Considerations, and Applications
- NADPH oxidase 1 promotes hepatic steatosis in obese mice and is abrogated by augmented skeletal muscle mass