GLP-1 receptor agonists and reduction of cardiometabolic risk: Potential underlying mechanisms
Open accessAbstract
Type 2 diabetes mellitus (T2DM) is a metabolic condition with an elevated impact on cardiovascular (CV) risk. The innovative therapeutic approaches for T2DM - incretin-based therapies (IBTs), including glucagon-like peptide 1 (GLP-1) receptor agonists, have become popular and more widely used in recent years. The available scientific data from clinical studies and clinical practice highlights their beyond glucose-lowering effects, which is achieved without any increase in hypoglycaemia. The former effects include reduction in body weight, lipids, blood pressure, inflammatory markers, oxidative stress, endothelial dysfunction, and subclinical atherosclerosis, thus reducing and potentially preventing CV events. In fact, the introduction of IBTs is one of the key moments in the history of diabetes research and treatment. Such therapeutic strategies allow customization of antidiabetic treatment to each patient's need and therefore obtain better metabolic control with reduced CV risk. The aim of the present paper is to provide a comprehensive overview of the effects of GLP-1RA on various cardiometabolic markers and overall CV risk, with particular attention on recent CV outcome studies and potential mechanisms. In particular, the effects of liraglutide on formation and progression of atherosclerotic plaque and mechanisms explaining its cardioprotective effects are highlighted.
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The cardiovascular benefits of GLP-1 receptor agonists cannot be explained merely by improved blood glucose control and weight loss.
“These benefits cannot be explained merely by improved blood glucose control and weight loss.97”
From The effect of <scp>GLP</scp> ‐1 receptor agonists on circulating inflammatory markers in type 2 diabetes patients: A systematic review and meta‐analysis (2025) · cites this paper as [97]
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“In addition, they have shown an antiatherogenic property both in animal models [95–98] and humans [99] (Figure 4).”
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- Authors
- Rizzo, M., Nikolic, D., Patti, A. M., Mannina, C., Montalto, G., McAdams, B. S., Rizvi, A. A., & Cosentino, F.
- Affiliations
- University of South Carolina (US)
- University of Palermo (IT)
- Karolinska University Hospital (SE)
- Corresponding author
- Rizzo, Manfredi
- ORCID
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2018-09
- Volume
- 1864
- Issue
- 9
- Pages
- 2814-2821
- ISSN
- 0925-4439 (ISSN-L)
- OpenAlex
- W2804938814
- Semantic Scholar
- 1fc14c6cefab0b97a4e6d33554079f967fa3585f
- Cited by
- 152
- References
- 78
- Citations by year
- 2026: 11 · 2025: 16 · 2024: 18 · 2023: 21 · 2022: 26 · 2021: 25 · 2020: 17 · 2019: 13 · 2018: 5
- FWCI
- 2.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- Nova Science Publishers (Nova Science Publishers, Inc.) (submittedVersion)
- CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- GLP-1 receptor agonists, type 2 diabetes, cardiometabolic risk, cardiovascular risk reduction, incretin-based therapy, liraglutide, atherosclerosis, atherosclerotic plaque, endothelial dysfunction, oxidative stress, inflammation, blood pressure, lipids, weight loss, cardioprotection
- MeSH terms
- Glucagon-Like Peptide-1 Receptor, Liraglutide, Glucagon-Like Peptide-1 Receptor Agonists, Semaglutide, Blood Glucose, Cardiovascular Diseases, Diabetes Mellitus, Type 2, Glucagon-Like Peptides, Humans, Hypoglycemic Agents, Incretins, Plaque, Atherosclerotic
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