Christopher L. Cunningham, Ph.D. is an Assistant Professor in the Departments of Otolaryngology and Neurobiology at the University of Pittsburgh School of Medicine, and a faculty member in the Pittsburgh Hearing Research Center. His research program focuses on the molecular mechanisms of hearing and deafness, with a particular emphasis on hereditary forms of hearing loss and the assembly, trafficking, and localization of mechanotransduction channel components in cochlear hair cells. The Cunningham Lab also develops gene therapies to treat congenital and acquired hearing loss.
Chris earned his Ph.D. in Neuroscience from the University of California, Davis in the lab of Dr. Stephen Noctor, and completed postdoctoral training in auditory neuroscience in the lab of Dr. Ulrich Müller at The Scripps Research Institute and Johns Hopkins School of Medicine. Chris has authored numerous highly cited peer-reviewed research articles, and his work is supported by multiple grants from the NIH and DOD, along with private foundation awards including from the Eye and Ear Foundation of Pittsburgh. He is a co-founder of Echogenesis Therapeutics, a biotech startup company focused on development of precision gene therapies for hearing and balance disorders. Chris is extremely fortunate to work with an amazing group of people in his lab, and he has been and continues to be inspired, motivated, and guided by many great scientists and mentors.
- Johns Hopkins University School of Medicine, Postdoctoral Fellowship in Neuroscience
- The Scripps Research Institute, Postdoctoral Fellowship in Neuroscience
- University of California, Davis, PhD in Neuroscience
- Brigham Young University, BS in Biology
Education & Training
X Qiu, JP Llongueras, L Yin, C Cunningham, U Müller. LHFPL5 is required for maximal activation of the mechanotransduction channel in cochlear hair cells. Proceedings of the National Academy of Sciences 122 (45), e2505627122
Sanzhaeva, U., Boyd-Pratt, H., Bender, P.T.R., Cunningham, C. et al. TUBB4B is essential for the cytoskeletal architecture of cochlear supporting cells and motile cilia development. Commun Biol 7, 1146 (2024). https://doi.org/10.1038/s42003-024-06867-2
Wang, P., Miller, K.K., He, E., Cunningham, C. et al. LOXHD1 is indispensable for maintaining TMC1 auditory mechanosensitive channels at the site of force transmission. Nat Commun 15, 7865 (2024). https://doi.org/10.1038/s41467-024-51850-4
B Bizup, S Brutsaert, CL Cunningham, A Thathiah, T Tzounopoulos. Cochlear zinc signaling dysregulation is associated with noise-induced hearing loss, and zinc chelation enhances cochlear recovery. Proceedings of the National Academy of Sciences 121 (8), e2310561121
Krey JF, Chatterjee P, Halford J, Cunningham CL, Perrin BJ, Barr-Gillespie PG (2023). Control of stereocilia length during development of hair bundles. PLoS Biol 21(4): e3001964. https://doi.org/10.1371/journal.pbio.3001964
The Cunningham Lab is interested in understanding the neural and sensory biology of the vertebrate auditory system. Many unique and highly specialized proteins with exquisitely precise subcellular localizations are critical for each step of sound processing. Hearing loss is the most common sensory deficit, and multiple forms of hearing loss involve aberrant proteostasis—improper assembly, trafficking, and/or regulation of key auditory proteins. The lab utilizes mouse models of human deafness for its experiments. The similarities between the rodent and human auditory systems allow for a panoply of experimental manipulations that aim to uncover basic biological mechanisms and translational insights relevant for human health. The lab utilizes cutting-edge techniques including the generation and analysis of novel genetic mouse models combined with biochemistry, molecular biology, histology, viral vectors and high-resolution fluorescent microscopic imaging. Ultimately, the hope is to utilize the findings toward the development of new therapies for hearing loss and deafness. To this end, the lab is developing gene therapy strategies that can treat hearing loss.