Area of research
Sensory Systems · Dermatology
Research interest
Research interests include Ion Channels and Receptors, Dermatology and Skin Diseases, Helicobacter pylori-related gastroenterology studies, and Pain Mechanisms and Treatments.
Phillyrin alleviates Kawasaki disease-induced lung inflammation by inhibiting platelet production through the NLRP3/IL-1β/NF-E2 signaling pathway
Enteric neuronal Piezo1 maintains mechanical and immunological homeostasis by sensing force
Water-soluble polysaccharides from citri reticulatae pericarpium alleviates LCWE-induced endothelial dysfunction by targeting TLR2-mediated NF-κB-NLRP3 pathway
Shexiang Tongxin Dropping Pills attenuate ischemic microvascular dysfunction via suppressing P66Shc-mediated mitochondrial respiration deficits
Astrocyte–neuron crosstalk through extracellular vesicle-shuttled miRNA-382-5p promotes traumatic brain injury
The Therapeutic Potential of Four Main Compounds of Zanthoxylum nitidum (Roxb.) DC: A Comprehensive Study on Biological Processes, Anti-Inflammatory Effects, and Myocardial Toxicity
Self-adhesion conductive cardiac patch based on methoxytriethylene glycol-functionalized graphene effectively improves cardiac function after myocardial infarction
A TRPV4-dependent neuroimmune axis in the spinal cord promotes neuropathic pain
MrgprA3-expressing pruriceptors drive pruritogen-induced alloknesis through mechanosensitive Piezo2 channel
Pharmacodynamics of frigid zone plant <i>Taxus cuspidata S. et Z.</i> against skin melanin deposition, oxidation, inflammation and allergy
Miswiring of Merkel cell and pruriceptive C fiber drives the itch-scratch cycle
Estrogen metabolites increase nociceptor hyperactivity in a mouse model of uterine pain
Nitidine chloride induces cardiac hypertrophy in mice by targeting autophagy-related 4B cysteine peptidase
TRPV4 is not the molecular sensor for bacterial lipopolysaccharides-induced calcium signaling
MrgprA3-expressing pruriceptors drive pruritogen-induced alloknesis through mechanosensitive Piezo2 channel
Piezo2 channel–Merkel cell signaling modulates the conversion of touch to itch
Sensory Neurons Co-opt Classical Immune Signaling Pathways to Mediate Chronic Itch
Transient receptor potential vanilloid 4–expressing macrophages and keratinocytes contribute differentially to allergic and nonallergic chronic itch