REVIEW article
Front. Nutr.
Sec. Nutrition and Metabolism
Volume 12 - 2025 | doi: 10.3389/fnut.2025.1661603
This article is part of the Research TopicPharmacodynamic and Pharmacokinetic Aspects of Redox Signaling in Inflammation-associated Damage and DiseasesView all articles
Metabolic Syndrome: Epidemiology, Mechanisms, and Current Therapeutic Approaches
Provisionally accepted
- 1Livingstone Center for Prevention and Translational Science, Livingstone, Zambia
- 2Mulungushi University, Kabwe, Zambia
- 3Vanderbilt University Medical Center, Nashville, United States
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Metabolic syndrome (MetS) is a complex condition marked by central obesity, dyslipidemia, hypertension, insulin resistance, oxidative stress, and chronic inflammation. These risk factors significantly raise the risk of cardiovascular disease (CVD) through various mechanisms, leading to a public health challenge. MetS contributes to CVD through cardiometabolic derangements such as endothelial dysfunction, atherosclerosis, oxidative stress, and inflammation. Dyslipidemia, especially elevated triglycerides and reduced high-density lipo-protein (HDL) cholesterol is central to atherosclerosis. Additionally, hypertension and insulin resistance damage blood vessels, a process exacerbated by chronic inflammation and oxidative stress. Thus, managing MetS and its components through lifestyle changes like weight control, dietary improvements, exercise, and smoking cessation is essential for reducing CVD risk. Medications targeting specific risk factors, such as blood sugar, cholesterol, and blood pressure, may also be required. Raising awareness and early screening are crucial to countering MetS's impact on public health. This review provides a comprehensive overview of the mechanisms by which MetS contributes to CVD and the intricate interplay of factors and molecular pathways linking MetS to CVD.
Keywords: metabolic syndrome, cardiovascular disease, Dyslipidemia, Insulin Resistance, Inflammation, Oxidative Stress, Obesity, Hypertension
Received: 10 Jul 2025; Accepted: 13 Aug 2025.
Copyright: © 2025 Hamooya, Siame, Muchaili, Masenga and Kirabo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Sepiso Kenias Masenga, Mulungushi University, Kabwe, Zambia
Annet Kirabo, Vanderbilt University Medical Center, Nashville, United States
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