Research Topic

Insulin Resistance, Metabolic Syndrome, and Cardiovascular Disease

About this Research Topic

Metabolic syndrome (MetS) is a leading public health and clinical challenge worldwide. MetS describes the co-occurrence of a collection of cardiometabolic risk factors including obesity, hypertension, and dyslipidemia. It has been established that those with MetS have three times higher risk of cardiovascular disease (CVD). So far, however, our understanding of MetS is limited, its underlying pathophysiological mechanisms and the interplay between the cardiometabolic risk factors and CVD remain to be further investigated.

Insulin resistance is defined as a suboptimal cellular response to physiological levels of insulin in diverse tissues, including liver, muscle, and adipose tissue. Insulin resistance impairs glucose disposal, resulting in compensatory hyperinsulinemia. The metabolic consequences of insulin resistance can result in hyperglycemia, dyslipidemia, hypertension, visceral adiposity, elevated inflammatory markers, endothelial dysfunction, and a prothrombic state. Therefore, insulin resistance plays a central role in the pathophysiology of MetS and increases the risk of CVD.

As the prevalence of MetS continues to increase worldwide, it is of critical importance to gain further insights into the interaction among MetS, insulin resistance, and CVD, as well as the prevention and treatment strategies of MetS. In this Research Topic, we would like to create a forum for current advances on cellular and physiological mechanisms linking insulin resistance, MetS, and CVD, as well as pathophysiological and clinical consequences of CVD induced by insulin resistance and MetS. We welcome manuscripts focusing on the molecular mechanisms involved in the development of insulin resistance and metabolic syndrome as well as the signaling and metabolic pathways in cardiovascular diseases. We also expect clinical or experimental studies evaluating the efficacy of potential therapeutics against insulin resistance and MetS in CVD.

Topics of interest include but are not limited to:
- Prevention and treatment options for insulin resistance and MetS which consequentially benefit cardiovascular disease patients
- The molecular mechanisms involved in the development of insulin resistance and metabolic pathways in CVDs, especially for hypertension, coronary heart disease, and heart failure.
- The role of insulin resistance in the pathogenesis of the MetS and its pathophysiological mechanisms in CVDs
- The effect of insulin resistance on lipid and lipoprotein metabolism in CVDs
- The effect of increased FFA flux mediated signal transduction in CVDs
- Insulin resistance and a pro-inflammatory / pro-thrombotic state in CVDs
- Other clinical correlations among insulin resistance, MetS, and CVDs


Keywords: Insulin Resistance, Metabolic Syndrome, Cardiovascular Disease, Diabetes, Risk Factors


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Metabolic syndrome (MetS) is a leading public health and clinical challenge worldwide. MetS describes the co-occurrence of a collection of cardiometabolic risk factors including obesity, hypertension, and dyslipidemia. It has been established that those with MetS have three times higher risk of cardiovascular disease (CVD). So far, however, our understanding of MetS is limited, its underlying pathophysiological mechanisms and the interplay between the cardiometabolic risk factors and CVD remain to be further investigated.

Insulin resistance is defined as a suboptimal cellular response to physiological levels of insulin in diverse tissues, including liver, muscle, and adipose tissue. Insulin resistance impairs glucose disposal, resulting in compensatory hyperinsulinemia. The metabolic consequences of insulin resistance can result in hyperglycemia, dyslipidemia, hypertension, visceral adiposity, elevated inflammatory markers, endothelial dysfunction, and a prothrombic state. Therefore, insulin resistance plays a central role in the pathophysiology of MetS and increases the risk of CVD.

As the prevalence of MetS continues to increase worldwide, it is of critical importance to gain further insights into the interaction among MetS, insulin resistance, and CVD, as well as the prevention and treatment strategies of MetS. In this Research Topic, we would like to create a forum for current advances on cellular and physiological mechanisms linking insulin resistance, MetS, and CVD, as well as pathophysiological and clinical consequences of CVD induced by insulin resistance and MetS. We welcome manuscripts focusing on the molecular mechanisms involved in the development of insulin resistance and metabolic syndrome as well as the signaling and metabolic pathways in cardiovascular diseases. We also expect clinical or experimental studies evaluating the efficacy of potential therapeutics against insulin resistance and MetS in CVD.

Topics of interest include but are not limited to:
- Prevention and treatment options for insulin resistance and MetS which consequentially benefit cardiovascular disease patients
- The molecular mechanisms involved in the development of insulin resistance and metabolic pathways in CVDs, especially for hypertension, coronary heart disease, and heart failure.
- The role of insulin resistance in the pathogenesis of the MetS and its pathophysiological mechanisms in CVDs
- The effect of insulin resistance on lipid and lipoprotein metabolism in CVDs
- The effect of increased FFA flux mediated signal transduction in CVDs
- Insulin resistance and a pro-inflammatory / pro-thrombotic state in CVDs
- Other clinical correlations among insulin resistance, MetS, and CVDs


Keywords: Insulin Resistance, Metabolic Syndrome, Cardiovascular Disease, Diabetes, Risk Factors


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

01 December 2020 Abstract
04 April 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

01 December 2020 Abstract
04 April 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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