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Insulin says NO to cardiovascular disease
Abstract
It is well recognized that insulin resistance found in patients with type 2 diabetes and obesity is a major risk factor for cardiovascular disease. Since its discovery in the 1920s, insulin has been used as an essential therapeutic agent in diabetes for blood glucose management. Recent studies demonstrate that insulin signalling is essential for normal cardiovascular function, and lack of it (i.e. insulin resistance) will result in cardiovascular dysfunction and disease. Moreover, insulin is the key component of glucose-insulin-potassium cocktail and exerts significant cardiovascular protective effect via a phosphatidylinositol 3'-kinase-protein kinase B-endothelial nitric oxide synthase (PI3K-Akt-eNOS)-dependent signalling mechanism in addition to its metabolic modulation, which renders it a potent organ protector in multiple clinical applications. This review focuses on insulin-initiated PI3K-Akt-eNOS survival signalling, with nitric oxide as an 'end effector' delivering cardioprotection in health and disease (especially in ischaemic heart disease), and highlights the impairment of this survival signalling as a key link between insulin resistance and cardiovascular disease.
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“The insulin receptor shares a signaling pathway with the activation of endothelial NOS (eNOS) [19,48,49,50,51,52] to regulate the postprandial blood flow and efficient nutrient disposition to peripheral tissues”
From NO-Rich Diet for Lifestyle-Related Diseases (2015) · cites this paper as [51]
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“mediated activation of NOS3 [185].”
Metadata
- Authors
- Yu, Q., Gao, F., & Ma, X. L.
- Affiliations
- Xijing Hospital (CN)
- Thomas Jefferson University (US)
- Corresponding author
- Gao, F.
- Ma, X. L.
- ORCID
- Yu, Q.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-11-04
- Volume
- 89
- Issue
- 3
- Pages
- 516-524
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W2019407178
- Semantic Scholar
- 7937e8f40b97ed3ed36508bc9198f0624094673d
- Cited by
- 172
- References
- 94
- Citations by year
- 2026: 7 · 2025: 3 · 2024: 9 · 2023: 7 · 2022: 12 · 2021: 10 · 2020: 10 · 2019: 6 · 2018: 8 · 2017: 8 · 2016: 11 · 2015: 14 · 2014: 20 · 2013: 16 · 2012: 23
- FWCI
- 1.53
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cardiovascular Research (publishedVersion)
- PubMed (publishedVersion)
- 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
- insulin resistance, cardiovascular disease, insulin signaling, PI3K/Akt/eNOS pathway, nitric oxide, cardioprotection, ischemic heart disease, type 2 diabetes, obesity, endothelial function
- MeSH terms
- Animals, Diabetic Angiopathies, Humans, Insulin, Insulin Resistance, Nitric Oxide, Myocardial Ischemia
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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