Area of research
Neurology · Molecular Biology
Research interest
Research focused on Microglia and Neuroscience, with related work in Cell biology, Substantia nigra, Gap junction. Notable publications include 'Rg1 improves LPS-induced Parkinsonian symptoms in mice via inhibition of NF-κB signaling and modulation of M1/M2 polarization', 'PARP14 inhibits microglial activation via LPAR5 to promote post-stroke functional recovery', and 'CKLF1 Aggravates Focal Cerebral Ischemia Injury at Early Stage Partly by Modulating Microglia/Macrophage Toward M1 Polarization Through CCR4'.
CKLF1 disrupts microglial efferocytosis following acute ischemic stroke by binding to phosphatidylserine
Tunneling nanotubes: The transport highway for astrocyte-neuron communication in the central nervous system
Ginsenoside Rg1 ameliorates stress-exacerbated Parkinson’s disease in mice by eliminating RTP801 and α-synuclein autophagic degradation obstacle
Correction: CKLF1 Aggravates Focal Cerebral Ischemia Injury at Early Stage Partly by Modulating Microglia/Macrophage Toward M1 Polarization Through CCR4
A breakdown of metabolic reprogramming in microglia induced by CKLF1 exacerbates immune tolerance in ischemic stroke
A novel small-molecular CCR5 antagonist promotes neural repair after stroke
A small molecule 20C from Gastrodia elata inhibits α-synuclein aggregation and prevents progression of Parkinson’s disease
A breakdown of metabolic reprogramming in microglia caused by CKLF1 exacerbates immune tolerance in the ischemic stroke
Neuronal chemokine-like-factor 1 (CKLF1) up-regulation promotes M1 polarization of microglia in rat brain after stroke
Pyk2 inhibition attenuates hypoxic-ischemic brain injury in neonatal mice
Rg1 improves LPS-induced Parkinsonian symptoms in mice via inhibition of NF-κB signaling and modulation of M1/M2 polarization
PARP14 inhibits microglial activation via LPAR5 to promote post-stroke functional recovery
CKLF1 Aggravates Focal Cerebral Ischemia Injury at Early Stage Partly by Modulating Microglia/Macrophage Toward M1 Polarization Through CCR4
Corticosterone impairs gap junctions in the prefrontal cortical and hippocampal astrocytes via different mechanisms
RTP801 is a critical factor in the neurodegeneration process of A53T α‐synuclein in a mouse model of Parkinson's disease under chronic restraint stress