Holly Van Remmen, PhD
- Research Program: Geroscience
- Position: Physiology, Member and Program Chair
Biography
Dr. Van Remmen is Member and Program Chair of the Aging and Metabolism Research Program at the Oklahoma Medical Research Foundation where she also holds the G.T. Blankenship Chair for Research in Aging. She is also Adjunct Professor of Physiology at the Oklahoma Health Sciences Center and a VA Senior Research Career Scientist at the Oklahoma City VA Medical Center. Her research program probes the role of oxidative stress and mitochondrial function in the biochemical and physiologic alterations that occur during aging, sarcopenia and neurodegenerative disease. She has authored over 180 scientific publications and has held a number of leadership and administrative positions. She served as President of the American Aging Association in 2006, was elected for a second term in 2022-2023 and was awarded the Denham Harman Lifetime Achievement Award from that Society. In 2009, she was Co-Chair of the Gordon Research Conference on Oxidative Stress and Disease held in Italy. Dr. Van Remmen is also currently Co-Director of the NIA-funded Oklahoma Nathan Shock Center and Leader of the Geroscience Redox Biology Core. She is also President of the Society for Redox Biology and Medicine (SFRBM) for 2020-2022.
Publications
- Graduate School
- Aging University of Texas Heath Science Center San Antonio
- Undergraduate School
- Zoology Eastern Illinois University
- Using transgenic and knockout models with modified antioxidant defense systems to test the role of oxidative stress and mitochondrial function in aging
- Studying the role of mitochondria and oxidative stress on motor neurons, the neuromuscular junction and skeletal muscle that might contribute to the significant problem of age-related loss of muscle mass and may have implications for onset and progression of ALS
- Studying the effect of the compound OKN-007 as a potential mediator of neuronal health and survival in the spinal cord in aging and neurodegenerative disease and how this might alter the loss of motor neuron function and downstream degenerative changes in skeletal muscle
- Investigating the potential for maintaining or enhancing cytosolic calcium homeostasis as a mechanism for preserving muscle mass through upregulation of the sarcoendoplasmic reticulum ATPase pump (SERCA) using a small molecule SERCA activator
- Understanding the role for hydroperoxides and pro-inflammatory pathways derived from arachidonic acid in modulating skeletal muscle mass.
- Reduced ADP sensitivity in skeletal muscle mitochondria increases ROS production in mouse models of aging and oxidative stress but not denervation 2021
- Neuron-specific deletion of CuZnSOD leads to an advanced sarcopenic phenotype in older mice 2020
- Targeting cPLA2 derived lipid hydroperoxides as a potential intervention for sarcopenia 2020
- Restoration of sarcoplasmic reticulum Ca2+ ATPase (SERCA) activity prevents age-related muscle atrophy and weakness in mice 2020
- Mitochondrial oxidative stress impairs contractile function but paradoxically increases muscle mass via fiber branching 2019
- Lifelong reduction in complex IV induces tissue specific metabolic effects but does not reduce lifespan or healthspan in mice 2018
- Dietary restriction attenuates age-associated muscle atrophy by lowering oxidative stress in mice even in complete absence of CuZnSOD 2012
- High rates of superoxide production in skeletal muscle mitochondria respiring on both Complex I and Complex II linked substrates 2008
- Absence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophy 2006
- Life-long reduction in MnSOD activity results in increased DNA damage and higher incidence of cancer but does not accelerate aging 2003