ArticleScientific reports2017
Tyrosine kinase inhibitors of Ripk2 attenuate bacterial cell wall-mediated lipolysis, inflammation and dysglycemia.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 39 citations in OpenAlex.
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- Advances in gut-lung axis research: clinical perspectives on pneumonia prevention and treatment.Frontiers in immunology · 2025Review
- NOD1: a metabolic modulator.Frontiers in endocrinology · 2024Review
- The tyrosine kinase inhibitor Dasatinib reduces cardiac steatosis and fibrosis in obese, type 2 diabetic mice.Cardiovascular diabetology · 2023Article
- NOD-like Receptors-Emerging Links to Obesity and Associated Morbidities.International journal of molecular sciences · 2023Review
- Activation of RIPK2-mediated NOD1 signaling promotes proliferation and invasion of ovarian cancer cells via NF-κB pathway.Histochemistry and cell biology · 2022Article
- Activation of NOD1 and NOD2 in the development of liver injury and cancer.Frontiers in immunology · 2022Review
- NOD1-Targeted Immunonutrition Approaches: On the Way from Disease to Health.Biomedicines · 2021Review
- Article
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- Knockdown of RIPK2 Inhibits Proliferation and Migration, and Induces ApoptosisFrontiers in genetics · 2021Article
- NOD1: An Interface Between Innate Immunity and Insulin Resistance.Endocrinology · 2019Review
- Article
- Inflammation promotes adipocyte lipolysis via IRE1 kinase.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation underpins aspects of insulin resistance and dysglycemia. Microbiota-derived cell wall components such as muropeptides or endotoxin can trigger changes in host immunity and metabolism. Specific peptidoglycan motifs promote metabolic tissue inflammation, lipolysis and insulin resistance via Nucleotide-binding oligomerization domain-containing protein 1 (Nod1). Receptor-interacting serine/threonine-protein kinase 2 (Ripk2) mediates Nod1-induced immunity, but the role of Ripk2 in metabolism is ill-defined. We hypothesized that Ripk2 was required for Nod1-mediated inflammation, lipolysis and dysglycemia. This is relevant because certain tyrosine kinase inhibitors (TKIs) inhibit Ripk2 and there is clinical evidence of TKIs lowering inflammation and blood glucose. Here, we showed that only a subset of TKIs known to inhibit Ripk2 attenuated Nod1 ligand-mediated adipocyte lipolysis. TKIs that inhibit Ripk2 decreased cytokine responses induced by Nod1-activating peptidoglycan, but not endotoxin in both metabolic and immune cells. Pre-treatment of adipocytes or macrophages with the TKI gefitinib inhibited Nod1-induced Cxcl1 and Il-6 secretion. Furthermore, treatment of mice with gefitinib prevented Nod1-induced glucose intolerance in vivo. Ripk2 was required for these effects on inflammation and metabolism, since Nod1-mediated cytokine and blood glucose changes were absent in Ripk2
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