ArticleEMBO reports2022
Endothelial-immune crosstalk contributes to vasculopathy in nonalcoholic fatty liver disease.
Article in EMBO reports, 2022. 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 9 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.
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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
9 citing papers in PubMed, 12 citations in OpenAlex.
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- The LIDPAD Mouse Model Captures the Multisystem Interactions and Extrahepatic Complications in MASLD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Unraveling the connection between Hashimoto's Thyroiditis and non-alcoholic fatty liver disease: exploring the role of CD4Endocrine · 2024Article
- Role of Perturbated Hemostasis in MASLD and Its Correlation with Adipokines.Life (Basel, Switzerland) · 2024Review
- Review
- Elucidating the genetic architecture of DNA methylation to identify promising molecular mechanisms of disease.Scientific reports · 2022Article
- Single-Cell Transcriptome of Wet AMD Patient-Derived Endothelial Cells in Angiogenic Sprouting.International journal of molecular sciences · 2022Article
- Endothelial-immune crosstalk contributes to vasculopathy in nonalcoholic fatty liver disease.EMBO reports · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The top cause of mortality in patients with nonalcoholic fatty liver disease (NAFLD) is cardiovascular complications. However, mechanisms of NAFLD-associated vasculopathy remain understudied. Here, we show that blood outgrowth endothelial cells (BOECs) from NAFLD subjects exhibit global transcriptional upregulation of chemokines and human leukocyte antigens. In mouse models of diet-induced NAFLD, we confirm heightened endothelial expressions of CXCL12 in the aortas and the liver vasculatures, and increased retention of infiltrated leukocytes within the vessel walls. To elucidate endothelial-immune crosstalk, we performed immunoprofiling by single-cell analysis, uncovering T cell intensification in NAFLD patients. Functionally, treatment with a CXCL12-neutralizing antibody is effective at moderating the enhanced chemotactic effect of NAFLD BOECs in recruiting CD8
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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.