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Junfang Wu, BM, PhD

Academic Title:


Primary Appointment:


Secondary Appointment(s):


Administrative Title:

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

Additional Title:

Associate Director, University of Maryland – Medicine Institute for Neuroscience Discovery (UM-MIND)


MSTF, 6-34D

Phone (Primary):

(410) 706-5189


(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


2010-present      Member Center for Shock, Trauma and Anesthesiology Research (STAR)

2023-present      Associate Director  University of Maryland – Medicine Institute for Neuroscience Discovery (UM-MIND)


Research/Clinical Keywords

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

Highlighted Publications

1. 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. doi: 10.1186/s12974-024-03082-y. PMID: 38581043.

2. Li Y, Khan N, Ritzel RM, Lei Z, Allen S, Faden AI, Wu J. Sexually dimorphic extracellular vesicle responses after chronic spinal cord injury are associated with neuroinflammation and neurodegeneration in the brain. Journal of Neuroinflammation, 2023, Aug 31;20(1):197. PMID: 37653491. 

3. 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. 

4. 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. doi: 10.1126/sciadv.add1101.

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

6. 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

7. Li Y, Ritzel RM, Lei Z, Cao T, He J, Faden AI, Wu J. Sex dimorphism in neurological function after SCI is associated with disrupted neuroinflammation in both injured spinal cord and brain. Brain, Behavior, and Immunity. 2022 Mar; 101: 1-22. PMID: 34954073

8. Dutta D, Khan N, Wu J#, Jay SM#. Extracellular Vesicles as an Emerging Frontier in Spinal Cord Injury Pathobiology and Therapy. Trends Neurosci. 2021 June: 44(6): 492-506. PMID: 33581883. (# correspondent)

9. Ritzel RM, He J, Li Y, Cao T, Khan N, Shim B, Sabirzhanov B, Aubrecht T, Stoica BA, Faden AI, Wu L-J, Wu J. Proton extrusion during oxidative burst in microglia exacerbates pathological acidosis following traumatic brain injury. Glia, 2021 Mar;69(3):746-764. PMID: 33090575.

10. 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

11. 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.

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Additional Publication Citations

1. Jakovceyski I, Wu J * (co-first author), Karl N, Leshchyns’ka I, Sytnyk V, Chen J, Irintchev A, Schachner M. Glial scar expression of CHL1, the close homolog of the adhesion molecule CHL1 limits recovery after spinal cord injury. Journal of Neuroscience, 2007, 27(27): 7222-7233.    **Highlighted by Nature Medicine

2. Wu J, Yoo S, Wilcock D, Lytle LM, Leung PY, Colton CA, Wrathall JR. Interaction of NG2+ glial progenitors and microglia/macrophages from the injured spinal cord. GLIA, 2010, 58(4):410-422.

3. Wu J, Renn CL, Faden AI, Dorsey SG. TrkB.T1 contributes to neuropathic pain following spinal cord Injury through regulation of cell cycle pathways. Journal of Neuroscience, 2013, 33(30):12447-12463. PMID: 23884949.

4. Wu J, Zhao Z, Sabirzhanov B, Stoica BA, Kumar A, Luo T, Skovira J, Fade AI. Spinal cord injury causes brain inflammation associated with cognitive and affective changes: role of cell cycle pathways. Journal of Neuroscience, 2014, 34(33): 10989-11006. PMID: 25122899.

5. Liu S, Sarkar C, Dinizo M, Faden AI, Koh EY, Lipinski MM, Wu J. Disrupted autophagy after spinal cord injury is associated with ER stress and neuronal cell death. Cell Death & Disease. 2015, 6: PMID: 25569099.

6. Wu J, Zhao Z, Zhu X, Renn CL, Dorsey SG, Faden AI. Cell cycle inhibition limits development and maintenance of neuropathic pain following spinal cord injury. Pain, 2016, 157(2):488-503. PMID: 26797506.

7. Wu J and Lipinski MM. Autophagy in neurotrauma: good or bad or dysregulated. Cells, 2019 Jul 10; 8(7): 693. doi: 10.3390/cells8070693.pii: PMID: 31295858. Review.

8. Sabirzhanov B, Matyas J, Coll-Miro M, Yu L, Faden AI, Stoica BA, Wu J. Inhibition of microRNA-711 limits Ang-1 and Akt changes, tissue damage, and neurological dysfunction after contusive spinal cord injury in mice. Cell Death & Disease, 2019, 10(11):839. PMID: 31685802.

9. Ritzel RM, Li Y, He J, Khan N, Doran S, Faden AI, and Wu J. Sustained neuronal and microglial alterations are associated with diverse neurobehavioral dysfunction long after experimental brain injury. Neurobiology of Disease, 2020; 136:104713. PMID: 31843705

10. Li Y, Ritzel RM, He J, Cao T, Sabirzhanov B, Li H, Liu S, Wu L-J, Wu J. The voltage-gated proton channel Hv1 plays a detrimental role in contusion spinal cord injury via extracellular acidosis-mediated neuroinflammation. Brain, Behavior, and Immunity, 2021, 91: 267-283. PMID: 33039662.

11. Zou L, He J, Gu L, Shahror RA, Li Y, Cao T, Zhu J, Wang S, Fan X, Wu J#, Chao W. Brain Innate Immune Response via Extracellular miRNA-TLR7 Sensing during Polymicrobial Sepsis. Brain, Behavior, and Immunity. 2022 Feb, 100: 10-24. PMID: 34808293.                    (# correspondent)

12. Ritzel RM, Wu J. Functional phenotyping of microglia highlights the dark relationship between chronic TBI and normal age-related pathology. Neural Regeneration Research, 2023; 18(4):811-813. PMID: 36204847









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

1. 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

2. NIH 2RF1 NS094527       Wu / Lipinski                      06/01/2016 - 05/31/2027

The Function and Mechanisms of Autophagy in Spinal Cord Injury                         

Role: Contact PI

3. NIH R01 NS110825       Junfang Wu/Long-Jun Wu     05/15/2020 - 04/30/2025

The Function and Mechanisms of Voltage-Gated Proton Channel Hv1 in Spinal Cord Injury

Role: Contact PI

4. NIH RF1 NS110637          Wu/ Jay                            09/01/2019 - 08/31/2024

Dementia after Spinal Cord Injury: Mechanisms and Therapeutic Targeting

Role: Contact PI

5. NIH 1R01NS110567         Chao/ Wu/ Zou                  05/01/2019 - 02/29/2025

Targeting Brain Inflammation and Neurological Dysfunction in Sepsis

Role: PD/PI

6. NIH 1R01NS110635          Faden/ Wu            NCE        04/01/2019 - 03/31/2025

Mechanism of Inflammatory Related Brain Dysfunction after Spinal Cord Injury

Role: PD/PI

7. NIH R01 2NR013601    Dorsey/ Wu/ Faden       NCE   03/21/2012 - 06/30/2024

Spinal Mechanisms Underlying SCI-Induced Pain: Implications for Targeted Therapy

Role: PD/PI

8. 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, learning and memory, depression/anxiety function), cell cultures (primary microglia, astrocytes, neurons; cell lines), adult microglia/macrophage isolation and FACS analysis, immunohistochemistry and state-of-the-art microscopy (light/fluorescence/confocal) and image analysis (stereology), biochemistry/molecular biology (qPCR, Western, etc).

Laboratory Personnel:

  • Yun Li, PhD, Research Associate
  • Fengshan Yu, MD, Research Associate
  • Xiangbing Wu, PhD, Research Associate
  • Zhuofan Lei, PhD, Post-doctoral Fellow
  • Balaji Krishnamachary, PhD, Post-doctoral Fellow
  • Daniela Lecca, PhD, Post-doctoral Fellow
  • Liwen Wei, MD, Postdoctoral Fellow
  • Zihui Wang, PhD, Postdoctoral Fellow
  • Hui Li, BM, MS, Research Assistant