A5045111736- Mitochondrial Function and Pathology
- ATP Synthase and ATPases Research
- Endoplasmic Reticulum Stress and Disease
- Adipose Tissue and Metabolism
- Autophagy in Disease and Therapy
- Cardiovascular Function and Risk Factors
- Cancer, Hypoxia, and Metabolism
- Cardiac Valve Diseases and Treatments
- Sexual function and dysfunction studies
- Heme Oxygenase-1 and Carbon Monoxide
- Temporomandibular Joint Disorders
- Signaling Pathways in Disease
- Virus-based gene therapy research
- Cardiomyopathy and Myosin Studies
- Urinary Bladder and Prostate Research
- Metabolism, Diabetes, and Cancer
- Bone Metabolism and Diseases
- Metalloenzymes and iron-sulfur proteins
- CAR-T cell therapy research
- Bone health and treatments
- Pulmonary Hypertension Research and Treatments
- Peroxisome Proliferator-Activated Receptors
- Viral gastroenteritis research and epidemiology
- Pancreatic function and diabetes
- Hormonal and reproductive studies
University of Alberta
2016-2022
UConn Health
2017
University of Chile
2012-2014
Advanced Center for Chronic Diseases
2013-2014
Instituto de Ciências Farmacêuticas
2011
Sanofi (Mexico)
2008
Cardiomyocyte hypertrophy has been associated with diminished mitochondrial metabolism. Mitochondria are crucial organelles for the production of ATP, and their morphology function regulated by dynamic processes fusion fission. The relationship between dynamics cardiomyocyte is still poorly understood. Here, we show that treatment cultured neonatal rat cardiomyocytes hypertrophic agonist norepinephrine promotes fission (characterized a decrease in mean volume an increase relative number...
The flux of Ca2+ from the endoplasmic reticulum (ER) to mitochondria regulates metabolism. Within tumor tissue, metabolism is frequently repressed, leading chemotherapy resistance and increased growth mass. Therefore, altered ER–mitochondria could be a cancer hallmark, but only few regulatory proteins this mechanism are currently known. One candidate redox-sensitive oxidoreductase TMX1 that enriched on mitochondria-associated membrane (MAM), site flux. Our findings demonstrate cells with low...
Endoplasmic reticulum (ER) homeostasis requires molecular regulators that tailor mitochondrial bioenergetics to the needs of protein folding. For instance, calnexin maintains mitochondria metabolism and mitochondria-ER contacts (MERCs) through reactive oxygen species (ROS) from NADPH oxidase 4 (NOX4). However, induction ER stress a quick rewiring adapt new energy needs. This machinery is not characterized. We now show oxidoreductase ERO1⍺ covalently interacts with kinase RNA-like (PERK) upon...
Cardiac hypertrophy is characterized by alterations in both cardiac bioenergetics and insulin sensitivity. Insulin promotes glucose uptake cardiomyocytes its use as a substrate for glycolysis mitochondrial oxidation order to maintain the high energy demands. stimulates Ca2+ release from endoplasmic reticulum, however, how this translates changes metabolism either healthy or hypertrophic not fully understood. In present study we investigated insulin-dependent signaling normal norepinephrine...
Control of Ca 2+ flow from the ER to mitochondria by calnexin balances output energy production pathways.
Insulin is a major regulator of glucose metabolism, stimulating its mitochondrial oxidation in skeletal muscle cells. Mitochondria are dynamic organelles that can undergo structural remodeling order to cope with these ever-changing metabolic demands. However, the process by which morphology impacts insulin signaling cells remains uncertain. To address this question, we silenced fusion proteins Mfn2 and Opa1 assessed insulin-dependent responses L6 rat We found fragmentation attenuates...
Cardiac hypertrophy is characterized by alterations in both cardiac bioenergetics and insulin sensitivity. Insulin promotes glucose uptake cardiomyocytes its use as a substrate for glycolysis mitochondrial oxidation order to maintain the high energy demands. stimulates Ca2+ release from endoplasmic reticulum, however, how this translates changes metabolism either healthy or hypertrophic not fully understood. In present study we investigated insulin-dependent signaling normal norepinephrine...
Structured Abstract Objective To study the effects of intermittent parathyroid hormone ( PTH [1‐34]) on mandibular condylar cartilage MCC ) and subchondral bone in adult female mice. Materials Methods Twenty‐two, 20‐week‐old mice were used for vivo experiments. The experimental (n=11) received daily intraperitoneal injections [1‐34] 3 weeks, while control (n = 11) 0.9% saline solution. Mice euthanized then micro‐computed tomography (micro‐ CT ); histology immunostaining carried out to assess...