ArticleInternational journal of biological sciences2024
Neuropeptide substance P attenuates colitis by suppressing inflammation and ferroptosis via the cGAS-STING signaling pathway.
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The neuropeptide in ischemic brain injury: insights, challenges, and horizon of targeted interventions.Journal of translational medicine · 2026Pooled it
- Microbial extracellular vesicles from min pigs remodel macrophage polarization via STING to sustain intestinal immune homeostasis.Gut microbes · 2026Article
- Taurochenodeoxycholic acid alleviates MPPIBRO neuroscience reports · 2026Article
- A mild photothermal-mediated neuroimmunomodulatory composite hydrogel reverses the inflammatory osteoclast precursor phenotype to promote osteoporotic bone defect healing.Bioactive materials · 2026Article
- cGAS-STING Modulates the NF-κB Pathway to Influence the Occurrence of Ulcerative Colitis-Associated Colorectal Cancer.Digestive diseases and sciences · 2026Article
- C3aR inhibition alleviates cerebral ischemia-reperfusion injury via STING-mediated ferroptosis through SLC7A11/GPX4.iScience · 2026Article
- Senkyunolide I Inhibits mtDNA-cGAS-STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Aldose reductase inhibition suppresses microglial endoplasmic reticulum stress and ferritinophagy in ischemic stroke.Acta pharmacologica Sinica · 2026Article
- cGAS/STING Signaling in Ulcerative Colitis: Mechanism and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- The emerging Nexus of STING signaling and ferroptosis: from mechanisms to therapeutic opportunities.Cell death discovery · 2026Review
- GPR84 aggravates lung inflammation through activating ZBP1-PANoptosome mediated PANoptosis following IAV infection.Cell death discovery · 2026Article
- Intestinal Epithelial Cell Ferroptosis in Ulcerative Colitis: Pathogenesis, Signaling Networks, and Therapeutic Implications.Current medical science · 2026Review
- Supramolecular self-assembled polyphenol nanoparticles alleviate osteoarthritis by inhibiting chondrocyte ferroptosis.Materials today. Bio · 2026Article
- Review
- Targeting the Cyclic GMP-AMP Synthase-Stimulator of Interferon Genes Pathway: An Emerging Therapeutic Strategy for Digestive Diseases.Clinical and translational gastroenterology · 2026Review
- Mitochondrial DNA as a driver of inflammation via the cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Enteric nervous system and inflammatory bowel disease.Gastroenterology report · 2026Review
- Epigenetic and post-translational regulatory networks of ferroptosis in the tumor immune microenvironment.Experimental hematology & oncology · 2026Review
- Ferroptosis inhibits cementoblast mineralization via cGAS-STING/GPX4 axis.Progress in orthodontics · 2026Article
- Loss of LXRβ Drives CD4Biomedicines · 2026Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropeptide substance P (SP) belongs to a family of bioactive peptides and regulates many human diseases. This study aims to investigate the role and underlying mechanisms of SP in colitis. Here, activated SP-positive neurons and increased SP expression were observed in dextran sodium sulfate (DSS)-induced colitis lesions in mice. Administration of exogenous SP efficiently ameliorated the clinical symptoms, impaired intestinal barrier function, and inflammatory response. Mechanistically, SP protected mitochondria from damage caused by DSS or TNF-α exposure, preventing mitochondrial DNA (mtDNA) leakage into the cytoplasm, thereby inhibiting the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway. SP can also directly prevent STING phosphorylation through the neurokinin-1 receptor (NK1R), thereby inhibiting the activation of the TBK1-IRF3 signaling pathway. Further studies revealed that SP alleviated the DSS or TNF-α-induced ferroptosis process, which was associated with repressing the cGAS-STING signaling pathway. Notably, we identified that the NK1R inhibition reversed the effects of SP on inflammation and ferroptosis via the cGAS-STING pathway. Collectively, we unveil that SP attenuates inflammation and ferroptosis via suppressing the mtDNA-cGAS-STING or directly acting on the STING pathway, contributing to improving colitis in an NK1R-dependent manner. These findings provide a novel mechanism of SP regulating ulcerative colitis (UC) disease.
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