A5035822095- Mitochondrial Function and Pathology
- Cardiovascular and exercise physiology
- Cardiovascular Function and Risk Factors
- Cardiac Ischemia and Reperfusion
- ATP Synthase and ATPases Research
- Physical Activity and Health
- Cardiovascular Effects of Exercise
- Endoplasmic Reticulum Stress and Disease
- Adipose Tissue and Metabolism
- Ion channel regulation and function
- Cellular transport and secretion
- Diet and metabolism studies
- Pancreatic function and diabetes
- Latin American Urban Studies
- Sports Performance and Training
- Cholesterol and Lipid Metabolism
- Metabolism, Diabetes, and Cancer
- Metabolism and Genetic Disorders
- Heart Failure Treatment and Management
- Adipokines, Inflammation, and Metabolic Diseases
- Aging, Health, and Disability
- Peroxisome Proliferator-Activated Receptors
- Diabetes Treatment and Management
- Social Sciences and Policies
- Health and Lifestyle Studies
University of Groningen
2021-2025
University Medical Center Groningen
2021-2025
University of Chile
2017-2023
Advanced Center for Chronic Diseases
2020-2023
Universidad Santo Tomás
2015-2016
Dirección de Investigación y Desarrollo
2016
Low-grade chronic inflammation plays a pivotal role in the pathogenesis of insulin resistance (IR), and skeletal muscle has central this condition. NLRP3 inflammasome activation pathways promote low-grade several tissues. However, direct link between IR not been reported. Here, we evaluated components their GLUT4 translocation impairment during IR. Male C57BL/6J mice were fed with normal control diet (NCD) or high-fat (HFD) for 8 weeks. The protein levels NLRP3, ASC, caspase-1, gasdermin-D...
A physiological increase in cardiac workload results adaptive remodeling, characterized by increased oxidative metabolism and improvements performance. Insulin-like growth factor-1 (IGF-1) has been identified as a critical regulator of growth, but its precise role cardiometabolic adaptations to stress remains unresolved. Mitochondrial calcium (Ca 2+ ) handling proposed be required for sustaining key mitochondrial dehydrogenase activity energy production during conditions, thus ensuring the...
Abstract Aims Sodium–glucose cotransporter 2 inhibitors (SGLT2i) improve cardiac performance and clinical outcomes in patients with heart failure, yet mechanisms underlying these beneficial effects remain incompletely understood. We sought to determine whether SGLT2i‐induced improvements function are dependent on increased oxidation of ketone bodies. Methods results employed a mouse model cardiac‐specific knock‐out the enzyme D‐β‐hydroxybutyrate dehydrogenase‐1 (BDH1 cko ), rendering mice...
ATPase inhibitory factor-1 (IF1) preserves cellular ATP under conditions of respiratory collapse, yet the function IF1 normal respiring is unresolved. We tested hypothesis that promotes mitochondrial dysfunction and pathological cardiomyocyte hypertrophy in context heart failure (HF). Methods results: Cardiac expression was increased mice humans with HF, downstream neurohumoral signaling pathways patterns resembled fetal-like gene program. Adenoviral wild-type primary cardiomyocytes resulted...
RESUMENLa transición epidemiológica observada en las últimas décadas ha implicado un aumento creciente de enfermedades crónicas, fenómeno asociados con el estilo vida la población, al modelo alimentario y sedentarismo, lo que predispone a obesidad resistencia insulina, condicionando patologías cardio metabólicas como hipertensión arterial dislipidemia, favoreciendo desarrollo del síndrome metabólico.El tratamiento consiste manejo farmacológico, mejoras los hábitos alimentarios incorporación...
Abstract A Kinase Interacting Protein 1 (AKIP1) is a signalling adaptor that promotes physiological hypertrophy in vitro. The purpose of this study to determine if AKIP1 cardiomyocyte vivo. Therefore, adult male mice with cardiomyocyte-specific overexpression (AKIP1-TG) and wild type (WT) littermates were caged individually for four weeks the presence or absence running wheel. Exercise performance, heart weight tibia length (HW/TL), MRI, histology, left ventricular (LV) molecular markers...
A Kinase Interacting Protein 1 (AKIP1) is a signalling adaptor that promotes mitochondrial respiration and attenuates oxidative stress in cultured cardiomyocytes. We sought to determine whether AKIP1 influences function the adaptation response exercise vivo. assessed respiratory capacity, as well electron microscopy targeted-proteomics hearts from mice with cardiomyocyte-specific overexpression of (AKIP1-TG) their wild type (WT) littermates. These parameters were also after four weeks...
Background : ATPase inhibitor factor-1 (IF1) preserves cellular ATP under conditions of respiratory collapse, yet the function IF1 normal respiring is unresolved. We tested hypothesis that promotes mitochondrial dysfunction and pathological cardiomyocyte hypertrophy in context heart failure (HF). Methods results Cardiac expression was increased mice humans with HF, downstream neurohumoral signaling pathways patterns resembled fetal-like gene program. Adenoviral wild type primary...
Heart rate variability and insulin resistance among obese malesBackground: analysis provides quantitative information about vagal sympathetic modulation of cardiac function.Aim: To analyze the relationship between heart in patients.Material Methods: Male participants were studied, divided 10 subjects aged 27 ± 2 years with a body mass index (BMI) 31.2 1.3 kg/m , 15 overweight 24 3 BMI 26.7 1.5 14 normal weight 21 22.5 . Resting was measured period 5 minutes. A spectral done measuring low...
Current heart failure (HF) therapy remains unable to substantially improve exercise capacity. Studies have shown that training has beneficial effects on the in both health and disease. How mitochondria respond this setting has, however, received less attention literature. These may include protective changes mitochondrial function adaptations substrate utilization. This review describes exercise-induced cardiac metabolism, including utilization their function. We conclude exercising HF...
<title>Abstract</title> Ischemic conditions can flip the action of mitochondrial ATP-synthase from an ATP producing to consuming enzyme. The protein ATPase inhibitory factor 1 (ATPIF-1) prevents reversal, thereby preserving during ischemia. Recent evidence suggests that ATPIF-1 may also have detrimental effects on calcium (Ca2+) handling and permeability transition pore (mPTP) opening under ischemic conditions, challenging conventional views function ATPIF-1. To determine role myocardial...