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Qitao Ran, Ph.D.

Professor

Department of Cell Systems and Anatomy

Currently seeking M.S. & Ph.D. students

Reactive oxygen species (ROS) such as superoxide and hydrogen peroxide are generated during metabolism by mitochondria and by enzymes such as lipoxygenases and NADPH oxidases. Although ROS at low levels may be beneficial by acting as secondary signaling molecules to regulate cellular functions, excessive amounts of ROS induce oxidative damages to cause cell injury and cell death. Neurons’ ravenous demand of energy necessitates high metabolic rates which result in high ROS production. Neurons also have a high load of lipids enriched with polyunsaturated fatty acids that are particularly vulnerable to attack by ROS. Pathological conditions such as accumulation of miss-folded proteins and inflammation can further exacerbate ROS generation in neurons. Indeed, increased ROS are well-demonstrated in neurodegenerative diseases such as Alzheimer’s disease (AD) and Amyotrophic Lateral Sclerosis (ALS), and oxidative damage is believed to be a key pathogenic factor for both. Despite this, antioxidants have so far been disappointing in clinical trials for treatments of neurodegenerative diseases.  The main research interest of Ran lab is to illustrate the key events/pathways triggered by ROS that are ultimately responsible for injury and demise of neurons. The goal of our investigation is to identify targets that can be exploited for developing efficacious treatments/interventions. For example, we recently showed that glutathione peroxidase (Gpx4), a master regulator of ferroptosis, is essential for the survival of neurons underlying ALS and AD, suggesting that those neurons are vulnerable to ferroptosis. We are currently trying to determine whether ferroptosis is a key mode of neuron degeneration in ALS and AD and whether ferroptosis and other cell death mechanisms can serve as targets for therapeutic development.