ArticleCell death discovery2022
Alpha-7 nicotinic acetylcholine receptor agonist alleviates psoriasis-like inflammation through inhibition of the STAT3 and NF-κB signaling pathway.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Decoding the Gut-Fat-Heart Axis: From Molecular Communication Networks to Clinical Translation Strategies.International journal of molecular sciences · 2026Review
- Transcriptomic Profiling of Psoriatic Lesions by Tape-Stripping Reveals Site-Specific Differences.Journal of clinical medicine · 2026Article
- Gut microbiota-induced perturbation in bile acids alter keratinocyte lipid metabolism via FXR-NQO1 signaling in psoriasis.Nature communications · 2026Article
- Activation of α7nAChR reduces inflammation and apoptosis, promoting muscle regeneration through the AKT-FOXO1 pathway.Cell death and differentiation · 2026Article
- Neuroimmune Interactions in Inflammatory Skin and Intestinal Diseases.Journal of inflammation research · 2026Review
- Qingre Liangxue Acupuncture for Psoriasis: A Cholinergic Neuroimmune Framework.International journal of general medicine · 2026Review
- Neuroimmune Crosstalk in Psoriasis: Mechanisms and Therapeutic Implications.Inflammation · 2025Review
- TFEB-mediated proinflammatory response in murine macrophages induced by acute Alpha7 nicotinic receptor activation.Journal of leukocyte biology · 2025Article
- Tobacco smoking and sarcoidosis revisited-Evidence, mechanisms, and clinical implications: a narrative review.Current medical research and opinion · 2025Review
- B cell-derived acetylcholine mitigates skin inflammation in mice through α9 nicotinic acetylcholine receptor-mediated signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Molecular Link Between Psoriasis and Depression-Update on Pathophysiology.International journal of molecular sciences · 2025Review
- S1PR3-driven positive feedback loop sustains STAT3 activation and keratinocyte hyperproliferation in psoriasis.Cell death & disease · 2025Article
- Kushe Tincture Ameliorates DNCB-Induced Atopic Dermatitis by Affecting NF-Kb/JAK-STAT3 Pathway: Bioinformatics Analysis and Animal Experiment Verification.Journal of inflammation research · 2025Article
- From arthritis to central sensitization: targeting the neuro-immune axis via microglial modulation in acupuncture treatment for Juvenile Idiopathic Arthritis-associated pain.Frontiers in immunology · 2025Review
- Autophagy in inflammatory bowel disease: immunization, etiology, and therapeutic potential.Frontiers in immunology · 2025Review
- Pathophysiological Roles of Ion Channels in Epidermal Cells, Immune Cells, and Sensory Neurons in Psoriasis.International journal of molecular sciences · 2024Review
- CYSLTR1 antagonist inhibits Th17 cell differentiation by regulating the NF-κB signaling for the treatment of psoriasis.International journal of biological sciences · 2024Article
- Glia Signaling and Brain Microenvironment in Migraine.Molecular neurobiology · 2023Review
- Potential uses of auditory nerve stimulation to modulate immune responses in the inner ear and auditory brainstem.Frontiers in integrative neuroscience · 2023Article
- Topical Donepezil for Cholinergic Modulation in Chronic Wound Repair.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyReview
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Psoriasis is a chronic inflammatory cutaneous disease; it has been discovered that stimulation of the nervous system increases susceptibility to psoriasis. Although the cholinergic anti-inflammatory pathway, which is mediated by the alpha-7 nicotinic acetylcholine receptor (α7nAChR), is critical for controlling multiple types of inflammation, its expression pattern and pathogenesis function in psoriatic lesioned skin tissue are unknown. We hereby analyzed the expression of α7nAchR in human and mouse psoriatic skin tissue. In vivo, PNU-282987 or Methyllycaconitine, a specific agonist or antagonist of α7nAchR, were administered to imiquimod (IMQ)-induced psoriatic mouse models. The macroscopic appearance and histopathological features of the psoriatic mice skin were evaluated. In addition, cell proliferation and differentiation markers were investigated. The level of pro-inflammatory cytokines released from the lesioned skin, as well as the activation of the relevant signaling pathways, were measured. Our findings indicated that psoriatic lesional skin expressed an increased level of α7nAChR, with its tissue distribution being primarily in skin keratinocytes and macrophages. In an IMQ-induced murine psoriasis model, α7nAChR agonist PNU-282987 treatment alleviated psoriasis-like inflammation by down-regulating the expression of multiple types of pro-inflammatory mediators and normalized keratinocyte proliferation and differentiation, whereas α7nAChR antagonist treatment exacerbated its effect. Mechanically, we observed that activation of the α7nAChR inhibited the activation of the STAT3 and NF-κB signaling pathways in in vitro cultured HaCaT cells induced by Th17-related cytokine IL-6/IL-22 or Th1-related cytokine TNF-α. Taken together, these findings demonstrate that attenuation of psoriatic inflammation via the cholinergic anti-inflammatory pathway is dependent on α7nAChR activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.