Valeria Cavalli, Ph.D.

Robert E. and Louise F. Dunn Professor of Biomedical Research
Hope Center for Neurological Disorders
Center of Regenerative Medicine

Neurosciences Program
Molecular Cell Biology Program
Developmental, Regenerative and Stem Cell Biology Program
Biochemistry, Biophysics, and Structural Biology Program

  • 314-362-3540

  • 314 362 0155

  • 922 McDonnell Sciences Bldg



  • axon regeneration, nerve injury, epigenetic, transcription, glia biology, neuroimmune mechanisms, spinal cord injury, optic nerve injury

  • Cellular, Molecular and Epigenetic control of axon regeneration

Research Abstract:

Permanent disabilities following central nervous system (CNS) injuries result from the failure of injured axons to regenerate and re-build functional connections. The poor regenerative capacity of mature CNS neurons remains a major problem in neurobiology and an unmet medical need. In contrast, axon regeneration and partial functional recovery can occur in injured peripheral nerves, providing an opportunity to identify the molecular and cellular mechanisms that control axon repair.

Research in the Cavalli laboratory focuses on elucidating the principles and mechanisms by which peripheral sensory neurons with cell body in dorsal root ganglia regenerate. The lab focuses on understanding how the epigenetic and transcriptional changes elicited in injured sensory neurons promote axon regeneration. The lab also study how satellite glial cells, which envelop the neuronal soma participate in the repair process. The lab is also interested in understanding how immune cells influence neurons and satellite glial cells responses to injury.

A broader understanding of the multi-cellular mechanisms associated with nerve repair may lead to strategies to improve recovery after nervous system injuries. The laboratory use a multifaceted approach in the mouse model system with the goal to manipulate novel pathways the lab discovers to improve regeneration in the injured CNS, such as after optic nerve injury or spinal cord injury. The lab also uses human tissue to determine if findings in the mouse model system are relevant to the physiology of human neurons and glia.

We are working on three main projects

1. Intrinsic mechanisms controlling axon regeneration

2. Role of the DRG microenvironment surrounding neuronal soma in axon regeneration

3. Targeted strategies to improve regeneration in the injured central nervous system.

Selected Publications:

Avraham O, Fend R, Ewan EE, Rustenhoven J, Zhao G, Cavalli C. Profiling sensory neuron microenvironment after peripheral and central axon injury reveals key pathways for neural repair. eLife. September 29, 2021; 10:e68457 doi: 10.7554/eLife.68457
Press release:

Trier AM, Mack MR, Fredman A, Tamari M, Ver Heul AM, Zhao Y, Guo cJ, Avraham O, Ford ZK, Oetjen LK, Feng J, Dehner C, Coble D, Badic A, Joshita S, Kubo M , Gereau 4th RW, Alexander-Brett J, Cavalli V, Davidson S, Hu H , Liu Q , Kim BS. (2021) 12IL-33 Signaling in Sensory Neurons Promotes Dry Skin Itch J Allergy Clin Immunol S0091-6749(21)01405-6.

Spears LD, Adak S, Dong G, Wei X, Spyropoulos G, Zhang Q, Yin L, Feng C, Hu D, Lodhi IJ, Hsu F-F, Rajagopal R, Noguchi KK, Halabi CM, Brier L, Bice AR, Lananna BV, Musiek ES, Avraham O, Cavalli V, Holth JK, Holtzman DM, Wozniak DF, Culver JP, Semenkovich CF. Endothelial ether lipids link the vasculature to blood pressure, behavior, and neurodegeneration. J Lipid Res. Apr 21, 2021; 62:100079. doi: 10.1016/j.jlr.2021.100079. Online ahead of print.

Pita-Thomas W, Mangetti Gonçalves T, Zhao G, Cavalli V. (2021) Genome-wide chromatin accessibility analyses provide a map for enhancing optic nerve regeneration. Scientific Reports (11), Article number: 14924

Ewan EE, Avraham O, Carlin D, Goncalves TM, Zhao G, Cavalli, V. Ascending dorsal column sensory neurons respond to spinal cord injury and downregulate genes related to lipid metabolism. Scientific Reports. January 11, 2021; 11(1):374.

Avraham O, Deng PY, Jones A, Kuruvilla R, Semenkovich CF, Klyachko VA, Cavalli V. Satellite glial cells promote regenerative growth in sensory neurons. Nature Communications, Sep 29, 2020; 11(1):4891.
Department of Neuroscience featured publication

Carlin D, Halevi A, Ewan EE, Moore A Cavalli V. Nociceptor deletion of Tsc2 enhances axon regeneration by inducing a conditioning injury response in dorsal root ganglia. eNeuro. Jun 25, 2020; 6(3). pii: ENEURO.0168-19.2019.

Pita Thomas W, Mahar M, Joshi A, Gan D, Cavalli V. HDAC5 promotes optic nerve regeneration in retinal ganglion cells. Exp Neurology. 2019; 317:271-283.

Mahar M, Cavalli V. Intrinsic mechanisms of neuronal axon regeneration. Nature Reviews Neuroscience. 2018; 19(6):323-337.

Oh YM, Mahar M, Ewan E, Leahy K, Zhao G, Cavalli V. Epigenetic regulator UHRF1 inactivates REST and growth suppressor gene expression via DNA methylation to promote axon regeneration. PNAS. 2018; 115(52):E12417-E12426.

Cho Y, Shin JE, Ewan EE, Oh YM, Pita-Thomas W, Cavalli V. Activating injury-responsive genes with hypoxia enhances axon regeneration through neuronal HIF-1α. Neuron. 2015; 18:720-34.

Cho Y, Park D, Cavalli V. Filamin A is required in injured axons for HDAC5 activity and axon regeneration. J Biol Chem. 2015; 290(37):22759-70.

Watt D, Dixit R, Cavalli V. JIP3 activates kinesin-1 motility to promote axon elongation. J Biol Chem. 2015; 290(25):15512-25.

Song W, Cho Y, Watt D, Cavalli, V. Tubulin-tyrosine ligase (TTL)-mediated increase in tyrosinated α-tubulin in injured axons is required for retrograde injury signaling and axon regeneration. J Biol Chem. 2015; 290(23):14765-75.

Cho Y and Cavalli V. HDAC signaling in neuronal development and regeneration. Curr Opin Neurobiol. 2014; 27:188-126.

Cho Y, Sloutsky R, Naegle KM and Cavalli V. Injury-induced HDAC5 nuclear export is essential for axon regeneration. Cell. 2013; 155:894-908.
Selected by Faculty of 1000. Highlighted article: Editor’s Choice Science Signaling, Nature Reviews in Neuroscience, and The Scientist.

Shin JE, Cho Y, Beirowski B, Milbrandt J, Cavalli V, DiAntonio A. Dual leucine zipper kinase is required for retrograde injury signaling and axonal regeneration. Neuron. 2012; 74:1015-1022. Highlighted article: Nix P, Bastiani M. Neuron. 2012; 74(6):961-963.`

Last Updated: 10/29/2021 11:52:20 AM

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