ArticleThe Journal of experimental medicine2014
MyD88-dependent interplay between myeloid and endothelial cells in the initiation and progression of obesity-associated inflammatory diseases.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 57 papers.
What it found
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Who cites it
57 citing papers in PubMed, 82 citations in OpenAlex.
- MyD88 in myeloid cells drives angiotensin II-induced vascular inflammation, is associated with prevalent heart failure, and predicts all-cause mortality in arterial hypertension.European heart journal open · 2026Article
- Lipid raft proteomics identify endothelial myosin-9 (MYH9) as a regulator of low-density lipoprotein transcytosis and atherosclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- MyD88 orchestrates fatty acid metabolism in tumor-associated macrophages and non-alcoholic fatty liver disease-related hepatocarcinogenesis.Frontiers in immunology · 2025Article
- Role of oxidative stress in post-burn wound healing.Burns & trauma · 2025Review
- Article
- The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration.Nature cardiovascular research · 2024Article
- Unraveling the complex roles of macrophages in obese adipose tissue: an overview.Frontiers of medicine · 2024Review
- MyD88 in myofibroblasts enhances nonalcoholic fatty liver disease-related hepatocarcinogenesis via promoting macrophage M2 polarization.Cell communication and signaling : CCS · 2024Article
- Unravelling monocyte functions: from the guardians of health to the regulators of disease.Discovery immunology · 2024Review
- Immunologic and inflammatory consequences of SARS-CoV-2 infection and its implications in renal disease.Frontiers in immunology · 2024Review
- History and future perspectives of adipose tissue macrophage biology.Frontiers in pharmacology · 2024Review
- New Insights into NF-κB Signaling in Innate Immunity: Focus on Immunometabolic Crosstalks.Biology · 2023Review
- MYD88 and Proinflammatory Chemokines in Aortic Atheromatosis: Exploring Novel Statin Effects.International journal of molecular sciences · 2023Article
- STAT3/NF‑κB decoy oligodeoxynucleotides inhibit atherosclerosis through regulation of the STAT/NF‑κB signaling pathway in a mouse model of atherosclerosis.International journal of molecular medicine · 2023Article
- Adipose tissue macrophages as potential targets for obesity and metabolic diseases.Frontiers in immunology · 2023Review
- Article
- Anti-inflammatory properties of lemon-derived extracellular vesicles are achieved through the inhibition of ERK/NF-κB signalling pathways.Journal of cellular and molecular medicine · 2022Article
- IL-1R-IRAKM-Slc25a1 signaling axis reprograms lipogenesis in adipocytes to promote diet-induced obesity in mice.Nature communications · 2022Article
- Proteomic networks associated with tumor-educated macrophage polarization and cytotoxicity potentiated by heat-killed tuberculosis.Scientific reports · 2022Article
- Hydrolyzed Proteins and Vegetable Peptides: Anti-Inflammatory Mechanisms in Obesity and Potential Therapeutic Targets.Nutrients · 2022Review
Corrections and comments
- Erratum issuedRansohoff, Richard M [added]
Authors and funding
20 authors at 6 institutions in 3 countries.
Funding
Abstract
Low-grade systemic inflammation is often associated with metabolic syndrome, which plays a critical role in the development of the obesity-associated inflammatory diseases, including insulin resistance and atherosclerosis. Here, we investigate how Toll-like receptor-MyD88 signaling in myeloid and endothelial cells coordinately participates in the initiation and progression of high fat diet-induced systemic inflammation and metabolic inflammatory diseases. MyD88 deficiency in myeloid cells inhibits macrophage recruitment to adipose tissue and their switch to an M1-like phenotype. This is accompanied by substantially reduced diet-induced systemic inflammation, insulin resistance, and atherosclerosis. MyD88 deficiency in endothelial cells results in a moderate reduction in diet-induced adipose macrophage infiltration and M1 polarization, selective insulin sensitivity in adipose tissue, and amelioration of spontaneous atherosclerosis. Both in vivo and ex vivo studies suggest that MyD88-dependent GM-CSF production from the endothelial cells might play a critical role in the initiation of obesity-associated inflammation and development of atherosclerosis by priming the monocytes in the adipose and arterial tissues to differentiate into M1-like inflammatory macrophages. Collectively, these results implicate a critical MyD88-dependent interplay between myeloid and endothelial cells in the initiation and progression of obesity-associated inflammatory diseases.
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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.