Ahn Bumsoo, PhD
- Research Program: Geroscience
- Position: OMRF, Aging and Metabolism Research Program, Research Assistant Member
Biography
"The goal of my research program is 1) to elucidate the mechanisms responsible for sarcopenia (the progressive loss of muscle mass and function with age), and 2) to eventually develop treatments that can mitigate symptoms of sarcopenia and age-associated chronic diseases.
Role of oxidative stress in sarcopenia: one of the consequences of aging is mitochondrial defects and oxidative stress. To test the causal role of oxidative stress in sarcopenia, we use gain-of-function and loss-of-function mouse models and modulate antioxidant genes in tissue-specific manner. My laboratory specifically focuses on the mitochondrial function because mitochondria are the primary source of free radicals, calcium handling, and ATP production with significant implications in the quality and quantity of skeletal muscle.
Therapeutic intervention for sarcopenia and cancer cachexia: currently there is no pharmacological treatment effective for sarcopenia or cancer cachexia, regardless of their significance in quality of life. My laboratory is currently investigating the therapeutic potential of ghrelin. Emerging evidence shows protective effects of unacylated ghrelin in multiple myopathies due to its anti-oxidative and anti-inflammatory properties in skeletal muscle and other tissues, including motor neurons. If unacylated ghrelin offers protection against these myopathies in animals, it would be an excellent candidate for clinical trials as it has an excellent safety profile in humans."
Publications
- Graduate School
- Exercise Physiology University of Florida, Gainesville, USA
- Exercise Physiology UNC Chapel Hill, NC, USA
- Undergraduate School
- Physical Education Yonsei University, Seoul, South Korea
- Reactive oxygen species
- Mitochondria
- Skeletal muscle
- Sarcopenia
- Cancer cachexia
- Neurogenic atrophy
- Excess reactive oxygen species lead to concentric hypertrophy and increased systolic function of the heart in mice lacking superoxide dismutase 1. 2021
- Cancer cachexia in a mouse model of oxidative stress. J Cachexia Sarcopenia Muscle. 2020
- Mitochondrial oxidative stress impairs contractile function but paradoxically increases muscle mass via fiber branching. J Cachexia Sarcopenia Muscle. 2019
- Using MRI to measure in vivo free radical production and perfusion dynamics in a mouse model of elevated oxidative stress and neurogenic atrophy. 2019
- Nrf2 deficiency exacerbates age-related contractile dysfunction and loss of skeletal muscle mass. Redox Biol. 2018
- NAD(P)H oxidase subunit p47phox is elevated and p47phox knockout prevents diaphragm contractile dysfunction in heart failure. 2015
- Phrenic nerve stimulation increases human diaphragm fiber force after cardiothoracic surgery. 2014
- Cancer cachexia decreases specific force and accelerates fatigue in limb muscle. 2013
- Diaphragm and ventilator dysfunction during cancer cachexia. 2013