Proyectos
- Julio 2021 - Julio 2023
Adjudicado
Creación de imágenes de super-resolución ultrasónicas en placentas humanas ex-vivo
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Co-Investigador/a
- Abril 2021 - Abril 2024
Adjudicado
Effects of eccentric, concentric and eccentric/concentric training on muscle function and mass, functional performance, cardiometabolic health, quality of life and molecular adaptations of skeletal muscle in COPD patients: a multicenter randomized trial
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Co-Investigador/a
- Noviembre 2019 - Octubre 2022
FinalizadoAgencia Nacional de Investigación y Desarrollo - ANID
Exercise stimulates autophagy by downregulation of NOX2 activity improving young and aged human skeletal muscle function
[vc_section el_class="container mx-auto align-items-center circle--pattern" css=".vc_custom_1648956589196{padding-top: 3rem !important;}"][vc_row el_class="pb-5"][vc_column][vc_wp_custommenu nav_menu="6"][uoh_breadcrumb_component automatic_breadcrumb="true"][uoh_title_component title_dropdown="big" title_decorator="true"]{{title}}[/uoh_title_component][vc_column_text css=""]During the past few decades average life expectancy has dramatically increased worldwide; specifically by 2050 the number of older adults will overcome the number of young people in Chile. This leads to a major challenge due to multiple chronic diseases highly prevalent in elderly. Aging process is defined as a series of time-dependent physiological changes that decrease reserve and functional capacity of skeletal muscle. Several studies have proposed that aging is caused by damage of macromolecules by reactive oxygen species (ROS) and decreased autophagy levels, a process that is essential for skeletal muscle regeneration, homeostasis and function. Exercise is a novel strategy used in elderly, which has shown to improve muscle mass, muscle function and decrease chronic diseases in old individuals. However, the molecular mechanisms and signaling pathways involved on the benefits of exercise in aged skeletal muscle are not completely clear. While exercise regulations of oxidative stress and autophagy have been studied separately, a direct interplay between exercise inducing autophagy via a ROS-dependent pathway has not yet been addressed in young or aged human skeletal muscle. Moreover, studies in human skeletal muscle examining the autophagy modulation after endurance exercise are limited and controversial. Although it is known that resting autophagy levels are decreased in aged skeletal muscle, the effects of acute exercise on skeletal muscle autophagy between young and older adults remain to be elucidated and could shed light on regulation of autophagy in humans. Additionally, it is also not known if a controlled exercise-training program can induce similar increases in autophagy levels in older adults. Recently, we have shown that the non-mitochondrial sources of ROS, NADPH oxidases 2 (NOX2), plays a major role in ROS production in skeletal muscle, both at rest and during contracting activity. Furthermore, our preliminary results show that NOX2 expression is increased during the aging process and strongly correlates with decreased autophagy levels detected in aged human skeletal muscle. Moreover, we also show that 12 weeks of endurance exercise training reduced the NOX2 levels in aged human muscle. We speculate that a decrease in NOX2 associated with a decrease in ROS levels in aged skeletal muscle induced by exercise training will improve aged muscle function by re-stablishing autophagy up to young skeletal muscle levels[/vc_column_text][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649209804184{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5"][vc_row el_class="container mx-auto align-items-center p-md-0 pt-5"][vc_column el_class="p-0"][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649210787516{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5 pb-md-5"][vc_row el_class="container mx-auto align-items-center"][vc_column][/vc_column][/vc_row][/vc_section]
Investigador/a Responsable
- Octubre 2013 - Octubre 2016
Ejecutado
Modulación de la autofagia por el receptor de inositol trifosfato (IP3R) en distrofia muscular de Duchenne
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Co-Investigador/a
