Endothelium as a gatekeeper of fatty acid transport
Open accessAbstract
The endothelium transcends all clinical disciplines and is crucial to the function of every organ system. A critical, but poorly understood, role of the endothelium is its ability to control the transport of energy supply according to organ needs. Fatty acids (FAs) in particular represent a key energy source that is utilized by a number of tissues, but utilization must be tightly regulated to avoid potentially deleterious consequences of excess accumulation, including insulin resistance. Recent studies have identified important endothelial signaling mechanisms, involving vascular endothelial growth factor-B, peroxisome proliferator-activated receptor-γ, and apelin, that mediate endothelial regulation of FA transport. In this review, we discuss the mechanisms by which these signaling pathways regulate this key endothelial function.
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Brain transport of fatty acids is elevated in individuals with metabolic syndrome.
“Brain transport of fatty acids is elevated in individuals with metabolic syndrome [48].”
From The menace of obesity to depression and anxiety prevalence (2022) · cites this paper as [48]
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Flagged first, then by citations
1 of the 100 references couldn’t be matched to a known paper.
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Organotypic vasculature: From descriptive heterogeneity to functional pathophysiology
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Intercellular Communication Lessons in Heart Failure
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Autologous Human Immunocompetent White Adipose Tissue‐on‐Chip
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Morphological and Functional Remodeling of Vascular Endothelium in Cardiovascular Diseases
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Endothelial Cell CD36 Reduces Atherosclerosis and Controls Systemic Metabolism
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Bifenthrin Induces Fat Deposition by Improving Fatty Acid Uptake and Inhibiting Lipolysis in Mice
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PATHOPHYSIOLOGICAL SIGNIFICANCE OF ENDOTHELIAL HETEROGENEITY
Markova, V. E., Shishkova, D. K., Frolov, A. V., & Malashicheva, A. (2025) · Complex Issues of Cardiovascular Diseases · doi:10.17802/2306-1278-2025-14-4-135-155
- Authors
- Mehrotra, D., Wu, J., Papangeli, I., & Chun, H. J.
- Affiliations
- Yale University (US)
- Corresponding author
- Chun, Hyung J.
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2014-02
- Volume
- 25
- Issue
- 2
- Pages
- 99-106
- ISSN
- 1043-2760 (ISSN-L)
- PMC
- PMC3946743
- OpenAlex
- W2055057583
- Cited by
- 60
- References
- 100
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 3 · 2023: 6 · 2022: 6 · 2021: 6 · 2020: 7 · 2019: 7 · 2018: 6 · 2017: 7 · 2016: 1 · 2015: 3 · 2014: 2
- FWCI
- 0.19
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- Servier
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL113005, HL-095654, HL113005, K08HL095654)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Keywords
- endothelium, fatty acid uptake, endothelial signaling, VEGF-B, PPARγ, apelin, insulin resistance, energy metabolism
- MeSH terms
- Apelin, Animals, Biological Transport, Diabetes Mellitus, Endothelium, Fatty Acids, Humans, Insulin Resistance, Obesity, Signal Transduction, Intercellular Signaling Peptides and Proteins, Vascular Endothelial Growth Factor B, PPAR gamma, Adipose Tissue, White
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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