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Luis F. Queme, MD, PhD

  • Instructor, UC Department of Anesthesia



Pain is usually the primary complaint of patients seeking healthcare. My research interests include peripheral mechanisms of pain development, the transition from acute to chronic pain and stress influences on pain development. As a former clinician, my work is focused on improving the quality of life for patients living with pain.

The current therapeutic options for patients suffering from chronic pain are frequently inadequate. Medication can produce severe side effects or is ineffective at treating pain. By understanding how pain is perceived at the peripheral level, our lab aims to prevent the development of chronic pain before it begins. Through this strategy, we are working to find more effective therapeutic options.

Our team recently produced a publication highlighting how peripheral sensory neurons that innervate muscle regulate both pain perception and cardiovascular responses to exercise. We discovered that a change in the expression of a single gene after ischemia could precipitate the development of increased pain and increased blood pressure in response to muscle activity.

As a PhD student, the Japanese Ministry of Education, Science and Culture awarded me a full scholarship. As a postdoctoral fellow at Cincinnati Children's, I was awarded a fellowship from the American Heart Association to study the development of ischemic myalgias. My work was presented at multiple national and international meetings, including multiple annual meetings of the Society for Neuroscience as well as the World Congress on Pain in 2016 and 2018. I have more than 12 years of research experience and began working at Cincinnati Children's in 2014.


Disruption of Hyaluronic Acid in Skeletal Muscle Induces Decreased Voluntary Activity via Chemosensitive Muscle Afferent Sensitization in Male Mice. Queme, LF; Dourson, AJ; Hofmann, MC; Butterfield, A; Paladini, RD; Jankowski, MP. eNeuro. 2022; 9.

In silico Identification of Key Factors Driving the Response of Muscle Sensory Neurons to Noxious Stimuli. Nagaraja, S; Queme, LF; Hofmann, MC; Tewari, SG; Jankowski, MP; Reifman, J. Frontiers in Neuroscience. 2021; 15.

Systemic Delivery of AAV-Fdxr Mitigates the Phenotypes of Mitochondrial Disorders in Fdxr Mutant Mice. Yang, L; Slone, J; Zou, W; Queme, LF; Jankowski, MP; Yin, F; Huang, T. Molecular Therapy - Methods and Clinical Development. 2020; 18:84-97.

Systemic administration of AAV-Slc25a46 mitigates mitochondrial neuropathy in Slc25a46-/- mice. Yang, L; Slone, J; Li, Z; Lou, X; Hu, Y; Queme, LF; Jankowski, MP; Huang, T. Human Molecular Genetics. 2020; 29:649-661.

A dual role for peripheral GDNF signaling in nociception and cardiovascular reflexes in the mouse. Queme, LF; Weyler, AA; Cohen, ER; Hudgins, RC; Jankowski, MP. Proceedings of the National Academy of Sciences of the United States of America. 2020; 117:698-707.

Sex differences and mechanisms of muscle pain. Queme, LF; Jankowski, MP. 2019; 11:1-6.

A single administration of Neurotropin reduced the elongated immobility time in the forced swimming test of rats exposed to repeated cold stress. Nasu, T; Kubo, A; Queme, LF; Mizumura, K. Behavioural Pharmacology. 2019; 30:547-554.

Sex differences in primary muscle afferent sensitization following ischemia and reperfusion injury. Ross, JL; Queme, LF; Lamb, JE; Green, KJ; Jankowski, MP. Biology of Sex Differences. 2018; 9.

A histone deacetylase 3-dependent pathway delimits peripheral myelin growth and functional regeneration. He, X; Zhang, L; Queme, LF; Liu, X; Lu, A; Waclaw, RR; Dong, X; Zhou, W; Kidd, G; Yoon, S; et al. Nature Medicine. 2018; 24:338-351.

Interleukin 1β inhibition contributes to the antinociceptive effects of voluntary exercise on ischemia/reperfusion-induced hypersensitivity. Ross, JL; Queme, LF; Lamb, JE; Green, KJ; Ford, ZK; Jankowski, MP. Pain. 2018; 159:380-392.