ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018
Toll-like receptor 2 and 4 have opposing roles in the pathogenesis of cigarette smoke-induced chronic obstructive pulmonary disease.
Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 77 citations in OpenAlex.
- Convergent death programs in chronic obstructive pulmonary disease: how pyroptotic and ferroptotic crosstalk reshapes therapeutic paradigms.Frontiers in immunology · 2026Review
- The possible mechanisms linking chronic obstructive pulmonary disease and coronary atherosclerosis based on coronary computed tomography angiography and animal experiments.Frontiers in physiology · 2026Article
- Taking its TOLL: the role of toll-like receptor 4 in human health and disease, and its potential as a therapeutic target.Frontiers in immunology · 2026Review
- Identification of Th17 Cell-Associated Biomarkers and Their Potential Regulatory Mechanisms in Chronic Obstructive Pulmonary Disease Through Integrated Bioinformatics Analysis and Machine Learning.International journal of chronic obstructive pulmonary disease · 2026Article
- Local and systemic effects in e-cigarette users compared to cigarette smokers, dual users, and non-smokers.Respiratory research · 2025Article
- The Role of Inflammation in the Pathogenesis of Comorbidity of Chronic Obstructive Pulmonary Disease and Pulmonary Tuberculosis.International journal of molecular sciences · 2025Review
- Cell death crosstalk in respiratory diseases: unveiling the relationship between pyroptosis and ferroptosis in asthma and COPD.Molecular and cellular biochemistry · 2025Review
- Immune markers for pulmonary aspergillosis in patients with chronic obstructive pulmonary disease: a narrative review.Frontiers in immunology · 2025Review
- MAP2K1 dampens cigarette smoke-induced inflammation via suppression of type I interferon pathway activation.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Ameliorating lipopolysaccharide induced acute lung injury with Lianhua Qingke: focus on pulmonary endothelial barrier protection.Journal of thoracic disease · 2024Article
- Assessment of NLRP3 inflammasome activation in patients with chronic obstructive pulmonary disease before and after lung transplantation.Immunologic research · 2024Article
- Astaxanthin attenuates cigarette smoke-induced small airway remodeling via the AKT1 signaling pathway.Respiratory research · 2024Article
- HDAC6-selective inhibitor CAY10603 ameliorates cigarette smoke-induced small airway remodeling by regulating epithelial barrier dysfunction and reversing.Respiratory research · 2024Article
- Altered levels of IFN-γ, IL-4, and IL-5 depend on theFrontiers in immunology · 2024Article
- TLR7 promotes smoke-induced experimental lung damage through the activity of mast cell tryptase.Nature communications · 2023Article
- Advanced models for respiratory disease and drug studies.Medicinal research reviews · 2023Review
- Cigarette Smoke Modulates Inflammation and ImmunityAntioxidants & redox signaling · 2023Review
- S100A1 expression is increased in spinal cord injury and promotes inflammation, oxidative stress and apoptosis of PC12 cells induced by LPS via ERK signaling.Molecular medicine reports · 2023Article
- Toll-like receptor-guided therapeutic intervention of human cancers: molecular and immunological perspectives.Frontiers in immunology · 2023Review
- ProbioticInternational journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 5 countries.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) is the third leading cause of morbidity and death and imposes major socioeconomic burdens globally. It is a progressive and disabling condition that severely impairs breathing and lung function. There is a lack of effective treatments for COPD, which is a direct consequence of the poor understanding of the underlying mechanisms involved in driving the pathogenesis of the disease. Toll-like receptor (TLR)2 and TLR4 are implicated in chronic respiratory diseases, including COPD, asthma and pulmonary fibrosis. However, their roles in the pathogenesis of COPD are controversial and conflicting evidence exists. In the current study, we investigated the role of TLR2 and TLR4 using a model of cigarette smoke (CS)-induced experimental COPD that recapitulates the hallmark features of human disease. TLR2, TLR4, and associated coreceptor mRNA expression was increased in the airways in both experimental and human COPD. Compared with wild-type (WT) mice, CS-induced pulmonary inflammation was unaltered in TLR2-deficient ( Tlr2
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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.