ReviewInflammopharmacology2019
Syk: a new target for attenuation of Helicobacter pylori-induced gastric mucosal inflammatory responses.
Review in Inflammopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Toll-like Receptor 4 Signaling Mediates Gastritis and Gastric Cancer.Current molecular medicine · 2025Review
- Immunomodulatory role of spleen tyrosine kinase in chronic inflammatory and autoimmune diseases.Immunity, inflammation and disease · 2023Review
- Nuciferine attenuates lipopolysaccharide-stimulated inflammatory responses by inhibiting p38 MAPK/ATF2 signaling pathways.Inflammopharmacology · 2022Article
- Impact of the microenvironment on the pathogenesis of mucosa-associated lymphoid tissue lymphomas.World journal of gastrointestinal oncology · 2022Review
- High expression of TREM2 promotes EMT via the PI3K/AKT pathway in gastric cancer: bioinformatics analysis and experimental verification.Journal of Cancer · 2021Article
- Role of spleen tyrosine kinase in liver diseases.World journal of gastroenterology · 2020Review
- Syk promotes phagocytosis by inducing reactive oxygen species generation and suppressing SOCS1 in macrophage-mediated inflammatory responses.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The magnitude of gastric mucosal inflammatory response to H. pylori relies primarily on the extent of its key endotoxin, LPS, engagement of Toll-like receptor-4 (TLR4) and the initiation of signal transduction events converging on mitogen-activated protein kinase (MAPK) and IκB complex (IKK) cascades. These cascades, in turn, exert their control over the assembly of transcription factors, NFκB and AP1, implicated in the induction of the expression of iNOS and COX-2 proinflammatory genes. The LPS-induced TLR4 activation and the ensuing phosphorylation of its intracellular tyrosine domain by Src-family kinases not only leads to recruitment to the cytoplasmic domain of TLR4 of adaptor molecules directly involved in propagation of the signaling cascades converging on MAPK and IKK, but also provides a propitious docking site for a non-receptor tyrosine kinase, spleen tyrosine kinase (Syk), the activation of which apparently leads to upregulation in the expression of proinflammatory genes. Here, we review the pathways engaged by H. pylori in the recruitment and interaction of Syk with TLR4 in gastric mucosa, and discuss the cascades involved in Syk-mediated amplification in proinflammatory signaling. We focus, moreover, on the potential role of drugs targeting Syk and TLR4 in the treatment of H. pylori-related gastric disease.
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Identifiers
What OpenQuestion holds
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.