ArticleCell death & disease2022
FAK mediates LPS-induced inflammatory lung injury through interacting TAK1 and activating TAK1-NFκB pathway.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 51 citations in OpenAlex.
- Cordycepin Alleviates Acute Lung Injury by Targeting TAK1 to Inhibit MAPK and NF-κB Signaling Pathways.Biomolecules · 2026Article
- The landscape of protein post-translational modifications in the pathogenesis of acute respiratory distress syndrome.Journal of thoracic disease · 2026Review
- Transfer factor alleviates bovine mastitis and protects mammary epithelial barrier via the TAK1/NF-κB/MLCK signaling axis.Journal of animal science · 2026Article
- Targeting the CD47-SIRPα Axis in Atherosclerosis: From Pathogenesis to Therapeutic Implications.Journal of inflammation research · 2026Review
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- Targeting Focal Adhesion Kinase in Lung Diseases: Current Progress and Future Directions.Biomolecules · 2025Review
- Macrophage Polarization in Heterotopic Ossification: Inflammation, Osteogenesis, and Emerging Therapeutic Targets.International journal of molecular sciences · 2025Review
- Sinapic Acid-Conjugated Gadolinium Complexes as Anti-Inflammatory Theranostic Agents That Target Transforming Growth Factor β‑Activated Kinase 1 (TAK1).ACS pharmacology & translational science · 2025Article
- Article
- Fisetin alleviates Salmonella typhimurium-induced colitis through the TLR2/TLR4-NF-κB pathway, regulating microbiota, and repressing intracellular bacterial proliferation by focal adhesion kinase.European journal of nutrition · 2025Article
- Targeting the Toll-like Receptor Signaling Pathway in Lung Cancer: Therapeutic Opportunities and Challenges.Current drug targets · 2025Review
- Neohesperidin Dihydrochalcone Alleviates Lipopolysaccharide-Induced Vascular Endothelium Dysfunction by Regulating Antioxidant Capacity.Immunity, inflammation and disease · 2024Article
- Ezrin drives adaptation of monocytes to the inflamed lung microenvironment.Cell death & disease · 2024Article
- Anti-Inflammatory Effects of Fermented and Aged Mountain-Cultivated Ginseng Sprouts via Suppression of MAPK-NF-κB Pathway in Lipopolysaccharide-Stimulated RAW264.7 Macrophages.Food science & nutrition · 2024Article
- Noncanonical functions of adhesion proteins in inflammation.American journal of physiology. Cell physiology · 2024Review
- Injectable hybrid hydrogels enable enhanced combination chemotherapy and roused anti-tumor immunity in the synergistic treatment of pancreatic ductal adenocarcinoma.Journal of nanobiotechnology · 2024Article
- Targeting thrombospondin-2 retards liver fibrosis by inhibiting TLR4-FAK/TGF-β signaling.JHEP reports : innovation in hepatology · 2024Article
- [Protective effect of FAK inhibitor PF-562271 against human umbilical vein endothelial cell injury induced by aging platelets].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Loss of 15-Lipoxygenase in Retinodegenerative RCS Rats.International journal of molecular sciences · 2024Article
- Rosavin Alleviates LPS-Induced Acute Lung Injure by Modulating the TLR-4/NF-κB/MAPK Singnaling Pathways.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI), characterized by inflammatory damage, is a major clinical challenge. Developing specific treatment options for ALI requires the identification of novel targetable signaling pathways. Recent studies reported that endotoxin lipopolysaccharide (LPS) induced a TLR4-dependent activation of focal adhesion kinase (FAK) in colorectal adenocarcinoma cells, suggesting that FAK may be involved in LPS-induced inflammatory responses. Here, we investigated the involvement and mechanism of FAK in mediating LPS-induced inflammation and ALI. We show that LPS phosphorylates FAK in macrophages. Either FAK inhibitor, site-directly mutation, or siRNA knockdown of FAK significantly suppresses LPS-induced inflammatory cytokine production in macrophages. FAK inhibition also blocked LPS-induced activation of MAPKs and NFκB. Mechanistically, we demonstrate that activated FAK directly interacts with transforming growth factor-β-activated kinase-1 (TAK1), an upstream kinase of MAPKs and NFκB, and then phosphorylates TAK1 at Ser412. In a mouse model of LPS-induced ALI, pharmacological inhibition of FAK suppressed FAK/TAK activation and inflammatory response in lung tissues. These activities resulted in the preservation of lung tissues in LPS-challenged mice and increased survival during LPS-induced septic shock. Collectively, our results illustrate a novel FAK-TAK1-NFκB signaling axis in LPS-induced inflammation and ALI, and support FAK as a potential target for the treatment of ALI.
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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.