The DOI matches its Crossref record; 109 of the 109 references it cites were found in a registry or an index.
The link between metabolic abnormalities and endothelial dysfunction in type 2 diabetes: an update
Open accessAbstract
Despite abundant clinical evidence linking metabolic abnormalities to diabetic vasculopathy, the molecular basis of individual susceptibility to diabetic vascular complications is still largely undetermined. Endothelial dysfunction in diabetes-associated vascular complications is considered an early stage of vasculopathy and has attracted considerable research interests. Type 2 diabetes is characterized by metabolic abnormalities, such as hyperglycemia, excess liberation of free fatty acids (FFA), insulin resistance and hyperinsulinemia. These abnormalities exert pathological impact on endothelial function by attenuating endothelium-mediated vasomotor function, enhancing endothelial apoptosis, stimulating endothelium activation/endothelium-monocyte adhesion, promoting an atherogenic response and suppressing barrier function. There are multiple signaling pathways contributing to the adverse effects of glucotoxicity on endothelial function. Insulin maintains the normal balance for release of several factors with vasoactive properties. Abnormal insulin signaling in the endothelium does not affect the whole-body glucose metabolism, but impairs endothelial response to insulin and accelerates atherosclerosis. Excessive level of FFA is implicated in the pathogenesis of insulin resistance. FFA induces endothelial oxidative stress, apoptosis and inflammatory response, and inhibits insulin signaling. Although hyperglycemia, insulin resistance, hyperinsulinemia and dyslipidemia independently contribute to endothelial dysfunction via various distinct mechanisms, the mutual interactions may synergistically accelerate their adverse effects. Oxidative stress and inflammation are predicted to be among the first alterations which may trigger other downstream mediators in diabetes associated with endothelial dysfunction. These mechanisms may provide insights into potential therapeutic targets that can delay or reverse diabetic vasculopathy.
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“Endothelial dysfunction is attributed to many causes, including oxidative stress, chronic inflammation, and endothelium activation, in diabetes, which exhibits excessive free fatty acid (FFA), insulin resistance, and/or hyperglycemia [216,217].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [216]
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Inflammation, stress, and diabetes
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Adipose tissue dysfunction in obesity, diabetes, and vascular diseases
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Activation of Protein Kinase C Isoforms and Its Impact on Diabetic Complications
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Combating oxidative stress in vascular disease: NADPH oxidases as therapeutic targets
Drummond, G. R., Selemidis, S., Griendling, K. K., & Sobey, C. G. (2011) · Nature Reviews Drug Discovery · doi:10.1038/nrd3403 · Cited by 899
Endothelial dysfunction and vascular disease
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Inflammatory mechanisms in the regulation of insulin resistance
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Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I
Paneni, F., Beckman, J. A., Creager, M. A., & Cosentino, F. (2013) · European Heart Journal · doi:10.1093/eurheartj/eht149 · Cited by 1,455
Endothelial dysfunction — A major mediator of diabetic vascular disease
Sena, C. M., Pereira, A. M., & Seiça, R. M. F. (2013) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2013.08.006 · Cited by 819
Inflammatory Links Between High Fat Diets and Diseases
Duan, Y., Zeng, L., Zheng, C., Song, B., Li, F., Kong, X., & Xu, K. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.02649 · Cited by 495
Lozano, I. I., der Werf, R. V., Bietiger, W., Seyfritz, E., Péronet, C., Pinget, M., Jeandidier, N., Maillard, É., Marchioni, E., Sigrist, S., et al. (2016) · Nutrition & Metabolism · doi:10.1186/s12986-016-0074-1 · Cited by 349
AMPK, Mitochondrial Function, and Cardiovascular Disease
Wu, S., & Zou, M.-H. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21144987 · Cited by 286
Metadata
- Authors
- Zhang, H., Dellsperger, K. C., & Zhang, C.
- Affiliations
- University of Missouri (US)
- Corresponding author
- Zhang, Hanrui
- Venue
- Basic Research in Cardiology
- Published
- 2011-12-22
- Volume
- 107
- Issue
- 1
- Pages
- 237-237
- ISSN
- 0003-9217 (ISSN-L)
- 0300-8428
- 1435-1803
- PMC
- PMC5512574
- OpenAlex
- W2019514289
- Cited by
- 144
- References
- 109
- Citations by year
- 2026: 10 · 2025: 9 · 2024: 7 · 2023: 6 · 2022: 11 · 2021: 7 · 2020: 6 · 2019: 5 · 2018: 11 · 2017: 7 · 2016: 15 · 2015: 11 · 2014: 10 · 2013: 16 · 2012: 12
- FWCI
- 1.30
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Basic Research in Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Heart Association
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL085119, R01HL077566)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Keywords
- endothelial dysfunction, type 2 diabetes, diabetic vascular disease, hyperglycemia, free fatty acids, insulin resistance, hyperinsulinemia, dyslipidemia, glucotoxicity, endothelial oxidative stress, endothelial cell apoptosis, endothelial inflammation, endothelial barrier function, atherosclerosis, insulin signaling, therapeutic target
- MeSH terms
- Animals, Diabetes Mellitus, Type 2, Endothelium, Vascular, Fatty Acids, Nonesterified, Humans, Hyperglycemia, Insulin Resistance, Vasomotor System
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