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Junfang Wu, BM, PhD

Matjasko Professorship in Anesthesiology Research

Academic Title:

Professor

Primary Appointment:

Anesthesiology

Secondary Appointment(s):

Neurobiology

Administrative Title:

Director of the Anesthesiology Center for Neuroscience Research; Associate Director of UM-MIND

Additional Title:

Vice-Chair for Translational Research, Department of Anesthesiology; Associate Director, University of Maryland - Medicine Institute for Neuroscience Discovery (UM-MIND)

Location:

MSTF, 6-34D

Phone (Primary):

(410) 706-5189

Fax:

(410) 706-1639

Education and Training

BM (Medicine): Jiangxi Medical College, China
MS (Pharmacology): Jiangxi Medical College, China
PhD (Neuropharmacology): Nanjing Medical University, China
Postdoctoral training: Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
Postdoctoral training: National Institutes of Health, Bethesda, MD

Biosketch

Dr. Junfang Wu earned her BM (Medicine) and MS (Pharmacology) at Jiangxi Medical College, China. She received her PhD in Neuropharmacology from Nanjing Medical University, China, and completed postdoctoral training at the Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, in Beijing, China.

Dr. Wu also completed postdoctoral training at the National Institutes of Health in Bethesda, MD. She has been a member of the Shock, Trauma, and Anesthesiology Research (STAR) Center since 2010. She currently serves as the Associate Director of the University of Maryland – Medicine Institute for Neuroscience Discovery (UM-MIND).

On June 25, 2025, Dr. Wu was awarded the Matjasko Professor of Anesthesiology Research.

Research/Clinical Keywords

Traumatic brain injury, spinal cord injury, aging, post-anesthesia/surgery, dementia, neuropathic pain, inflammation, neuroprotection, autophagy-lysosomal, extracellular vesicles, Hv1/NOX2/ROS, TrkB.T1, motor function, cognition, depression, olfaction, microglia, neurons, astrocytes

Highlighted Publications

Lei Z, Li Y, Li H, Wu J. Autophagy activation by the Becn1F121A mutation reprograms neuroinflammation and promotes neurological recovery after spinal cord injury. Brain, Behavior, and Immunity, 2026 Jan;131:106191. doi: 10.1016/j.bbi.2025.106191. Online ahead of print. PMID: 41271189

Wang Z, Li Y, Lee HJ, Lei Z, Wu L-J, Wu J. Hv1 upregulation worsens spinal, spleen, and lung molecular pathology and impairs locomotion after spinal cord injury in aged male mice. Aging and disease, 2025, Dec 15. doi: 10.14336/AD.2025.1122. Online ahead of print. PMID: 41400580

Li Y, Uzun C, Islam ST, Krishnamachary, Lee H, Wang Z, Li H, Liu S, Wu J. Age-dependent transcriptional and circuit alterations in the brain underlie post-anesthesia neurobehavioral dysfunction. Aging and disease, 2025. June 06, PMID: 40540720. doi: 10.14336/AD.2025.0596. Online ahead of print. 

Ritzel RM, Li Y, Jiao Y, Doran SJ, Khan N, Henry RJ, Brunner K, Loane DJ, Faden AI, Szeto G, Wu J. Bi-directional neuro-immune dysfunction after chronic experimental brain injury. Journal of Neuroinflammation, 2024 Apr 5;21(1):83. PMID: 38581043.

Lei Z, Krishnamachary B, Khan NZ, Ji Y, Li Y, Li H, Brunner K, Faden AI, Jones JW, Wu J. Spinal cord injury disrupts plasma extracellular vesicles cargoes leading to neuroinflammation in the brain and neurological dysfunction in aged male mice. Brain, Behavior, and Immunity, 2024 Aug, 120: 584-603. PMID: 38986724. **Highlighted by BBI

Ritzel RM, Li Y, Jiao Y, Lei Z, Doran S, He J, Shahror RA, Henry RJ, Khan R, Tan C, Liu S, Stoica BA, Faden AI, Szeto G, Loane DJ, Wu J. Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with inflammatory neurodegeneration. Science Advances, 2023, Mar 10; 9(10): eadd1101. PMID: 36888713.

Liu X, Lei Z, Gilhooly D, He J, Li Y, Ritzel RM, Li H, Wu L-J, Liu S, Wu J. Traumatic brain injury-induced inflammatory changes in the olfactory bulb disrupt neuronal networks leading to olfactory dysfunction. Brain, Behavior, and Immunity, 2023, Aug 7, 114: 22-45. PMID: 37557959. 

Choi HMC, Li Y, Suraj D, Hsia RC, Wu J#, Lipinski MM#. Autophagy protein ULK1 interacts with and regulates SARM1 during axonal injury. PNAS, 2022 Nov 22; 119(47): e2203824119. PMID: 36375051. (# Correspondent)

Li Y, Lei Z, Ritzel RM, He J, Li H, Choi HMC, Lipinski MM, Wu J. Impairment of autophagy in spinal cord injury exacerbates neuroinflammation and motor functional deficits in mice. Theranostics, 2022; 12(12): 5364-5388. PMID: 35910787

Khan N, Cao T, He J, Ritzel RM, Li Y, Henry RJ, Colson C, Stoica1 BA, Faden AI, Wu J. Spinal cord injury alters microRNA and CD81+ exosome levels in plasma extracellular nanoparticles with neuroinflammatory potential. Brain, Behavior, and Immunity, 2021; 92:165-183. PMID: 33307173. **Highlighted by BBI

Li Y, Ritzel RM, Khan N, Cao T, He J, Matyas JJ, Sabirzhanov B, Liu S, Li H, Stoica BA, Loane DJ, Faden AI, Wu J. Delayed microglial depletion after spinal cord injury reduces chronic inflammation and neurodegeneration in the brain and improves neurological recovery in male mice. Theranostics, 2020; 10(25): 11376-11403. PMID: 33052221.

https://pubmed.ncbi.nlm.nih.gov/?term=junfang+wu+at+maryland&sort=date

https://pubmed.ncbi.nlm.nih.gov/?term=junfang+wu+at+new+jersey&sort=date

 

Additional Publication Citations

Research Interests

Neuroinflammation and Neuroprotection Following CNS Trauma

The focus of research in Dr. Wu’s laboratory is to understand the cellular and molecular mechanisms of neurological dysfunction following spinal cord injury (SCI) and traumatic brain injury (TBI), with the ultimate goal of developing potentially therapeutic strategies. In particular, we are interested in pathological mechanisms including disruption of autophagy and lysosomal pathway, astrocytic TrkB.T1, microglial Hv1 channel, NOX2, extracellular vesicles (EVs), and their contribution to neuroinflammation and neurodegeneration in both acute CNS trauma and aging conditions including chronic SCI/TBI and Alzheimer’s disease and related dementia (AD/ADRD).

Specifically, we focus on:

  1. Demonstrating the function and the mechanisms of autophagy-lysosomal pathway in SCI.
  2. Elucidating molecular mechanisms responsible for SCI-induced brain neuroinflammation and neurodegeneration.
  3. Investigating the role of plasma and tissue extracellular vesicles (EVs) in secondary injury after CNS trauma.
  4. Examining the function and mechanism of voltage-gated proton channels Hv1 on neuroinflammation and neuropathic pain after experimental SCI and TBI.
  5. Elucidating the inflammatory mechanisms underlying olfactory dysfunction in TBI model and its correlation with late-onset dementia-related pathology. 

Multidisciplinary approaches include rodent models of SCI and TBI, diverse behavioral evaluation, characterization of EVs, quantitative image analysis, as well as molecular and cellular biology.

Grants and Contracts

NIH R01 NS145443   Wu / Gan                                                     08/01/2025 - 07/31/2030
Mechanisms and intervention of cGAS signaling in brain trauma-induced neuroinflammation and neurodegeneration
Role: Contact PI

NIH RF1 AG093965    Ying / Wu                                                    09/15/2025 - 06/30/2030
Olfactory dysfunction as predictor of PM2.5 exposure progression to dementia
Role: MPI

NIH R01 AG077541   Wu / Liu                                                       06/15/2022- 03/31/2027
Inflammatory Mechanisms Underlying Olfactory Dysfunction in Prognosis of TBI Progression to Dementia
Role: Contact PI

NIH 2RF1 NS094527  Wu / Lipinski                                               06/01/2016 - 05/31/2027
The Function and Mechanisms of Autophagy in Spinal Cord Injury
Role: Contact PI

NIH R01 NS110825 (NCE)    Wu                                                    05/15/2020 - 04/30/2026
The Function and Mechanisms of Voltage-Gated Proton Channel Hv1 in Spinal Cord Injury
Role: PI

NIH R01NS119275      Kristian                                                       07/01/2021 - 06/30/2026
Using NAD+ Precursor for Treatment of Global Cerebral Ischemia
Role: Co-I

Lab Techniques and Equipment

A diverse array of in vivo and in vitro experimental models is used to study pathophysiological mechanisms of SCI and TBI. These include:

  • contusion spinal cord injury (mouse & rat)
  • controlled cortical impact (mouse)
  • behavioral analysis (mechanical/thermal pain, facial spontaneous pain, locomotor/motor, cognition, depression/anxiety function, olfactory function)
  • EVs characterization and cargo analysis (miRNAs, Proteomics, Lipidomics)
  • cell cultures (primary microglia, astrocytes, neurons; cell lines)
  • adult microglia/astrocytes isolation
  • FACS analysis, immunohistochemistry and state-of-the-art microscopy (light/fluorescence/confocal)
  • image analysis (stereology)
  • biochemistry/molecular biology (qPCR, Western, etc)

Laboratory Personnel:

  • Yun Li, PhD, Research Associate
  • Zhuofan Lei, PhD, Research Associate
  • Balaji Krishnamachary, PhD, Post-doctoral Fellow
  • Zihui Wang, PhD, Post-doctoral Fellow
  • Songah Chae, Ph.D., M.S., ATC., Post-doctoral Fellow
  • Hui Li, BM, MS, Research Assistant
  • Ruth Park, Medical student