Department of Cellular and Structural Biology

CSB Faculty


Qitao Ran, Ph.D.

Associate Professor


Peking Union Medical College, 1995


MED, 552C.4
(210) 567-3842


The main interest of my lab is to investigate the roles of mitochondrial dysfunction and oxidative stress in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease, ALS and brain aging. The ultimate goal of my research is to identify new therapeutic targets for neurodegenerative diseases.


Antioxidant defense enzymes, such as glutathione peroxidase 4 (Gpx4), peroxiredoxin 3 (Prdx3), glutaredoxin 2 (Glrx2), are essential for protecting mitochondria from damage caused by reactive oxygen species (ROS). My lab has generated transgenic and knockout mouse models that under- or over- express these antioxidant defense enzymes. By studying neuron dysfunction and pathologies in these animals, we can decipher mechanistic contributions of mitochondrial oxidative stress in disease pathogenesis. For example, we showed that the conditional deletion of Gpx4 in adult animals results in rapid neuron degeneration in spinal cord and brain. Further studies uncovered a new mechanism of neuron degeneration in these models. Our research using Prdx3 transgenic mice also demonstrated that mitochondrial ROS play a key role in cognitive impairment and Aβ accumulation in brain. Using whole animals as well as cultured cells, we are continuing to investigate the specific mechanisms of mitochondrial oxidative stress in neural injury and disease pathogenesis.

  • Biology of Aging, CSBL 6048, 6049 & 6050
  • INTD5000 Fundamentals of Biomedical Sciences
  • CSBL6021, Animal Models
Recent Publications:
Chen L, Hambright WS, Na R, Ran Q. Ablation of ferroptosis inhibitor glutathione peroxidase 4 in neurons results in rapid motor neuron degeneration and paralysis. J Biol Chem. 2015 Sep 23.


Chen L, Na R, Boldt E, Ran Q. NLRP3 inflammasome activation by mitochondrial reactive oxygen species plays a key role in long-term cognitive impairment induced by paraquat exposure. Neurobiol Aging. 2015 Sep;36(9):2533-43.


Chen L, Na R, Ran Q. Enhanced defense against mitochondrial hydrogen peroxide attenuates age-associated cognition decline. Neurobiol Aging. 2014 Nov;35(11):2552-61.


Yoo SE, Chen L, Na R, Liu Y, Rios C, Van Remmen H, Richardson A, Ran Q. Gpx4 ablation in adult mice results in a lethal phenotype accompanied by neuronal loss in brain. Free Radic Biol Med. 2012 May 1;52(9):1820-7.


Chen L, Yoo SE, Na R, Liu Y, Ran Q. Cognitive impairment and increased Aβ levels induced by paraquat exposure are attenuated by enhanced removal of mitochondrial H(2)O(2). Neurobiol Aging. 2012 Feb;33(2):432.e15-26.


Representative Publications:
Liang H, Yoo SE, Na R, Walter CA, Richardson A, Ran Q. Short form glutathione peroxidase 4 is the essential isoform required for survival and somatic mitochondrial functions. J Biol Chem. 2009 Nov 6;284(45):30836-44.


Chen L, Na R, Gu M, Salmon AB, Liu Y, Liang H, Qi W, Van Remmen H, Richardson A, Ran Q. Reduction of mitochondrial H2O2 by overexpressing peroxiredoxin 3 improves glucose tolerance in mice. Aging Cell. 2008 Dec;7(6):866-78.


Chen L, Na R, Gu M, Richardson A, Ran Q. Lipid peroxidation up-regulates BACE1 expression in vivo: a possible early event of amyloidogenesis in Alzheimer's disease. J Neurochem. 2008 Oct;107(1):197-207.