Publications

Selected Publications

(# co-first author or co-corresponding author)

TGFβ signaling mediates microglial resilience to spatiotemporally restricted myelin degeneration

Zhu K, Liu Y, Min J-H, Joshua V, Lin J, Li Y, Kreutzmann J.C., Guo Y, Xia W, Mohammadi E, Pieber M, Suerth V, Xia Y, Andrusivova Z, Hugnot J-P, Kanatani S, Ulhén P, Lundeberg J, Li X, Fancy SPJ, Sarlus H, Harris RA, Lund H.

Nature Neuroscience (2026)

Takeaway: TGFβ signaling acts as a region-specific protective checkpoint that maintains microglial resilience and prevents age-related myelin degeneration in the spinal cord dorsal column, revealing previously unrecognized spatial heterogeneity in microglia–oligodendrocyte interactions relevant to aging and neurodegenerative disease.

Expansion of outer cortical Cux2 neurons requires adaptations for DNA repair

Xia W, Morcom L, Xu Z, Lu IL, Wang Q, Hoi KK, Wei M, Zhu K, Jordan G, Tang X, Gonzalez Maya J, Mattera V, Panigrahi S, Kawaguchi R, Emery B, Franco SJ, Geschwind D, Popko B, Rowitch DH, Fancy SPJ.
Nature (2026)

Takeaway: The evolutionary expansion of higher-order L2/3 cortical CUX2+ neurons depends on an enhanced DNA-repair program driven by ATF4, which protects rapidly dividing neural progenitors from lethal DNA damage during brain development.

DNA damage burden causes selective CUX2 neuron loss in neuroinflammation

Morcom L, Xia W, Xu Z, Awasthi Y, Geywitz C, Ellis MO, Noli T, Zulji A, Yamamoto D, Girdler GC, Kai L, Zhu K, Wei M, Tang XY, Hoi KK, Gonzalez Maya J, Duncan GJ, Vaquie AM, Gold Diaz D, Kawaguchi R, Liu E, Sun Y, Yang D, Jordan G, Lu IL, Holmqvist S, Bartels T, Ridley K, Choi JJ, Franco SJ, Huang EJ, Emery B, Geschwind D, Schirmer L, Balmus G, Popko B, Fancy SPJ, Rowitch DH.

Nature (2026)

Takeaway: High DNA damage burden and inadequate repair in CUX2+ L2/3 excitatory neurons render them selectively vulnerable to degeneration during neuroinflammatory injury, with implications for the progression of multiple sclerosis.

Sanguinarine modulates microglial function via PPARγ activation and protects against CNS demyelination

Wang D, Wang X, Li S, Zhang T, Yang Y, Wang Y, Zhao X, Li K, Wang YQ, Li Y, Zhu K#, Wang J#.

International Immunopharmacology (2024)

Takeaway: Plant-derived alkaloid Sanguinarine offers a promising dual-action therapeutic approach for CNS demyelinating diseases by modulating microglia to reduce inflammation and promote myelin repair through PPARγ activation

Activation of TRPV1 receptor facilitates myelin repair following demyelination via the regulation of microglial function

Sun J#, Zhu K#, Wang Y#, Wang D, Zhang M, Sarlus H, Benito-Cuesta I, Zhao X, Zou Z, Zhong Q, Feng Y, Wu S, Wang Y, Harris RA, Wang J.

Acta Pharmacologica Sinica (2023) (COVER STORY)

Takeaway: TRPV1 activation reprograms microglia toward a pro-regenerative state that enhances myelin debris clearance, supports OPC differentiation, and promotes remyelination after demyelinating injury.

Myeloid cell-specific topoisomerase 1 inhibition using DNA origami mitigates neuroinflammation

Zhu K, Wang Y, Sarlus H, Geng K, Nutma E, Sun J, Kung S, Bay C, Han J, Benito-Cuesta I, Lund H, Amor S, Wang J, Zhang XM, Kutter C, Guerreiro Cacais A.O., Högberg B, Harris RA.

EMBO Reports (2022)

Takeaway: Topoisomerase 1 (TOP1) upregulation prevails in inflammatory microglial states and CNS demyelination. A myeloid-specific self-assembling DNA origami scaffold (MyloGami) loaded with the FDA-approved topotecan (TopoGami) functions as a myeloid-targeted TOP1 inhibitor with potent microglia-modulatory effects in CNS inflammatory demyelination.

Gsta4 controls apoptosis of differentiating adult oligodendrocytes during homeostasis and remyelination via the mitochondria-associated Fas-Casp8-Bid-axis

Carlström K, Zhu K, Ewing E, Krabbendam I, Harris RA, Falcão A, Jagodic M, Castelo-Branco G, Piehl F.

Nature Communications (2020)

Takeaway: Gsta4 promotes oligodendrocyte survival and remyelination by detoxifying mitochondrial lipid peroxidation products (notably 4-HNE) and suppressing the Fas–Casp8–Bid apoptotic pathway during oligodendrocyte differentiation, identifying Gsta4 as a potential reparative target in multiple sclerosis.

Absence of microglia or presence of peripherally-derived macrophages does not affect tau pathology in young or old hTau mice

Zhu K, Pieber M, Han J, Blomgren K, Zhang XM, Harris RA, Lund H.

Glia (2020)

Takeaway: Early-stage Alzheimer’s-like tau aggregation alone is insufficient to drive pathogenic microglial activation. Tauopathy can progress largely independently of microglia or infiltrating macrophages, implying that microglial contribution to Alzheimer’s disease may require a disease-activated inflammatory state rather than merely the presence or absence of myeloid cells.

miR-124/VAMP3 is a novel therapeutic target for the mitigation of surgical trauma-induced microglial activation

Chen Y, Sun J, Chen W, Wu G, Wang Y, Zhu K#, Wang J#.

Signal Transduction and Targeted Therapy (2019)

Takeaway: The miR-124/VAMP3 axis is a key regulator of surgical trauma–induced microglial activation. Electroacupuncture-induced upregulation of miR-124 suppresses pro-inflammatory microglial responses by targeting VAMP3-mediated vesicular trafficking, thereby mitigating postoperative neuroinflammation.

Repurposing of omeprazole for oligodendrocyte differentiation and remyelination

Zhu K, Sun J, Kang Z, Zou Z, Wu X, Wang Y, Wu G, Harris RA, Wang J.

Brain Research (2019)

Takeaway: In silico drug screening using Connectivity Map identifies omeprazole as a clinically available drug that promotes oligodendrocyte differentiation by activating ERK1/2 and p38 MAPK.

Full Publication List

Full Publication List