​Holly Van Remmen, Ph.D.


​​Postdoctoral Fellow 1995, University of Texas Health Science Center, Texas

PhD 1991, University of Texas Health Science Center, Texas

BS 1983, Eastern Illinois University, Illinois

Research Overview

There are two interconnected lines of research in the Van Remmen laboratory. The first is the study of how oxidative stress and mitochondrial function modulate age-related loss of skeletal muscle mass and function (sarcopenia), neuromuscular degeneration (Amyotrophic Lateral Sclerosis (ALS)) and changes in motor neurons in aging and neuromuscular disease.  Our research uses mouse models of altered oxidative stress and mitochondrial function to probe these pathways. We utilize a number of experimental approaches from in vivo assessment of animal behavior, motor function, neuronal and muscle function to approaches in cell culture, tissue samples or in isolated mitochondria. At the biochemical level, we interrogate pathways involved in aging and disease using molecular approaches to measure changes in mRNA and proteins. Finally, the Van Remmen laboratory is also a Core facility in the Nathan Shock Center for Excellence in the Biology of Aging.

​Van Remmen Lab

​Holly Van Remmen, Ph.D.

​Principal Investigator

​Bumsoo Ahn, Ph.D.

​​Research Assistant Member

​Shylesh Bhaskaran, Ph.D.

​Staff Scientist

​Kavithalakshmi Sataranatarajan, Ph.D

​​Staff Scientist

​Jacob Brown, Ph.D.

​​Post Doctoral Fellow

​Yang Xu, Ph.D.

​​Post Doctoral Fellow

​​Gavin Pharaoh, Ph.D.

​Post Doctoral Fellow

​Rojina Ranjit

​Research Assistant

​Ashley Murphy

​Senior Laboratory Technician

​Ryan McIntire

Research Technician

Lauren Oliver

Research Technician

Parker Kneis

Affiliate, Research Technician

​Kat Piekarz

​Graduate Student


​​Oklahoma Medical Research Foundation

​825 NE 13th Street, Chapman Building S108-S112

Oklahoma City OK 73104

Lab Phone: (405) 271-2653

​Office Phone: (405) 271-2​520


CV Link


Sarcopenia and the neuromuscular junction

My research program overall is focused on the role of oxidative stress and mitochondrial function in aging. In past studies, we utilized a number of transgenic and knockout models with modified antioxidant defense systems to ask whether changes in antioxidant defense and oxidative stress modify lifespan as predicted by the long-standing Oxidative Stress Theory of Aging. In contrast to the predictions of this Theory, our studies found that modifying antioxidant defenses does not alter lifespan, suggesting that oxidative stress may not be a primary factor underlying aging. However, we propose the oxidative stress is indeed a critical factor in age-associated diseases such as sarcopenia and Amyotrophic Lateral Sclerosis (ALS). Our recent work has focused on 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 using conditional knockout mouse models with tissue specific reduction in mitochondrial and cytosolic antioxidants.  These models allow us to probe neuronal versus muscle specific oxidative stress effects. We are also interested in age-related changes in the spinal cord that may be contributing to loss of motor neuron function and downstream degenerative changes in skeletal muscle.  Other studies in the lab are focused on 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 and the role for hydroperoxides and pro-inflammatory pathways derived from arachidonic acid in modulating skeletal muscle mass.