analyzing-oxygen-consumption-rate-primary-cultured-mouse-neonatal

Analyzing Oxygen Consumption Rate in Primary Cultured Mouse Neonatal Cardiomyocytes Using an Extracellular Flux Analyzer

Mitochondria and oxidative metabolism are critical for maintaining cardiac muscle function. Research has shown that mitochondrial dysfunction is an ...

University of California San Diego

Immobilization, bed rest, or denervation leads to muscle disuse and subsequent skeletal muscle atrophy. Muscle atrophy can also occur as a component of various chronic diseases such as cancer, AIDS, sepsis, diabetes, and chronic heart failure or as a direct result of genetic muscle disorders. In addition to this atrophic loss of muscle mass, metabolic deregulation of muscle also occurs. In contrast, physical exercise plays a beneficial role in counteracting disuse-induced atrophy by increasing muscle mass and strength. Along with this, exercise can also reduce mitochondrial dysfunction and metabolic deregulation. Still, while exercise causes valuable metabolic and functional adaptations in skeletal muscle, the mechanisms and effectors that lead to these changes such as increased mitochondria content or enhanced protein synthesis are not fully understood. Therefore, mechanistic insights may ultimately provide novel ways to treat disuse induced atrophy and metabolic deregulation. Mass spectrometry (MS)-based proteomics offers enormous promise for investigating the molecular mechanisms underlying disuse and exercise-induced changes in skeletal muscle. This review will focus on initial findings uncovered by using proteomics approaches with human skeletal muscle specimens and discuss their potential for the future study.

A mini review: Proteomics approaches to understand disused vs. exercised human skeletal muscle.

Inflammation is associated with cardiac remodeling and heart failure, but how it is initiated in response to nonischemic interventions in the absence of cell death is not known. We tested the hypothesis that activation of Ca/calmodulin-dependent protein kinase II δ (CaMKIIδ) in cardiomyocytes (CMs) in response to pressure overload elicits inflammatory responses leading to adverse remodeling.

Inflammation and NLRP3 Inflammasome Activation Initiated in Response to Pressure Overload by Ca/Calmodulin-Dependent Protein Kinase II δ Signaling in Cardiomyocytes Are Essential for Adverse Cardiac Remodeling.

Yoshitake Cho

Division of Cardiology,
Department of Medicine,
Division of Cardiology, Department of Medicine

University of California San Diego

Analyzing Oxygen Consumption Rate in Primary Cultured Mouse Neonatal Cardiomyocytes Using an Extracellular Flux Analyzer

Yoshitake Cho

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Division of Cardiology,Department of Medicine,Division of Cardiology, Department of Medicine

University of California San Diego

Analyzing Oxygen Consumption Rate in Primary Cultured Mouse Neonatal Cardiomyocytes Using an Extracellular Flux Analyzer

Division of Cardiology,
Department of Medicine,
Division of Cardiology, Department of Medicine