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 and brain aging. The ultimate goal of my research is to identify new therapeutic targets for neurodegenerative diseases and brain aging.


Antioxidant defense enzymes, such as glutathione peroxidase 4 (Gpx4), peroxiredoxin 3 (Prdx3), glutaredoxin 2 (Glrx2), are essential for protecting mitochondria from damage induced by reactive oxygen species. My lab has generated a series of transgenic and knockout mouse models that under- or over- express these antioxidant defense enzymes. By studying brain dysfunction and pathologies associated with Alzheimer's disease in these animals, we can decipher mechanistic contributions of mitochondrial oxidative stress in disease pathogenesis. For example, we showed that knockout of Gpx4, an antioxidant defense enzyme important in protecting mitochondrial membranes from oxidative damage, causes neurodegeneration in brain. And we showed that mitochondria H2O2 plays a key role in cognitive impairment and Aβ accumulation in brain using Prdx3 transgenic mice. Using whole animals as well as cultured cells from the mice, we are investigating the specific roles of mitochondrial oxidative stress on neural injury and cognition impairment.


I am also interested in understanding the role of toxin exposure in Alzheimer's disease pathogenesis, because emerging epidemiological data indicate that exposure to environmental toxins may elevate the risk of Alzheimer's disease. Using Alzheimer's disease mouse models and animal models generated in my lab, we are studying how toxin exposure may lead to decreased cognition and overproduction of Aβ.

  • Biology of Aging, CSBL 6048, 6049 & 6050
  • Fundamentals of Biomedical Sciences, INTD5000
  • Animal Models, CSBL6021
Recent Publications:
Koulajian K, Ivovic A, Ye K, Desai T, Shah A, Fantus IG, Ran Q., Giacca A. Overexpression of glutathione peroxidase 4 prevents β-cell dysfunction induced by prolonged elevation of lipids in vivo. Am J Physiol Endocrinol Metab. 2013 Jul 15;305(2):E254-62.


Sun Y, Li W, Lu Z, Chen R, Ling J, Ran Q., Jilka RL, Chen XD. Rescuing replication and osteogenesis of aged mesenchymal stem cells by exposure to a young extracellular matrix. FASEB J. 2011 May;25(5):1474-85.


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, 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.


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.


Representative Publications:
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.