Introduction: organ involvement in the cardiometabolic syndrome
Melvin R Hayden1, Craig S Stump, James R Sowers
1Department of Internal Medicine, Division of Endocrinology, Diabetes and Metabolism, Diabetes and Cardiovascular Disease Research Center, University of Missouri School of Medicine, Columbia, MO 65212, USA. mrh29@usmo.com
Insights
Cardiometabolic syndrome increases risks for type 2 diabetes, cardiovascular disease, and kidney disease. This overview details its clinical complications and organ remodeling, using the MINER acronym for key areas.
Area of Science:
- Cardiology
- Endocrinology
- Nephrology
- Hepatology
Background:
- Cardiometabolic syndrome (CMS) is a cluster of conditions including obesity, hypertension, dyslipidemia, and insulin resistance.
- CMS significantly elevates the risk of developing type 2 diabetes mellitus (T2DM), cardiovascular diseases (CVD), and chronic kidney disease (CKD).
- It also encompasses metabolic hepatopathy, such as nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH).
Purpose of the Study:
- To provide a comprehensive overview of the clinical complications associated with cardiometabolic syndrome.
- To review the cellular and extracellular matrix remodeling events in end-organs affected by CMS.
- To utilize the MINER acronym (Myocardial and metabolic-hepatopathy, Intimal and islet, Neurovascular, Endothelial, Renal oxidation-reduction (redox) stress and remodeling) as a framework for discussion.
Main Methods:
- Literature review and synthesis of existing research on cardiometabolic syndrome.
- Analysis of clinical data and pathological findings related to CMS complications.
- Conceptual framework development using the MINER acronym to organize key aspects of CMS.
Main Results:
- CMS is a complex syndrome involving multiple organ systems, leading to significant morbidity and mortality.
- Key complications include T2DM, various CVDs (coronary artery disease, peripheral arterial disease, stroke), CKD, and NAFLD/NASH.
- Cellular and extracellular matrix remodeling, driven by oxidation-reduction (redox) stress, is a critical mechanism underlying end-organ damage in CMS.
Conclusions:
- Cardiometabolic syndrome represents a critical intersection of metabolic, cardiovascular, renal, and hepatic pathologies.
- Understanding the end-organ remodeling processes is crucial for developing effective therapeutic strategies.
- The MINER framework provides a structured approach to comprehending the multifaceted nature of cardiometabolic syndrome and its sequelae.
Abstract:
The cardiometabolic syndrome is a construct associated with an increased risk of type 2 diabetes mellitus, cardiovascular disease (coronary artery disease, peripheral arterial disease, and stroke), chronic kidney disease, and the metabolic hepatopathy referred to as nonalcoholic fatty liver disease or nonalcoholic steatohepatitis. Thus, the term cardiometabolic syndrome includes all of these metabolic, islet, cardiovascular, renal, and hepatic disorders and clustering clinical syndromes. This overview of the cardiometabolic syndrome is designed to review the clinical complications and the end-organ cellular and extracellular matrix remodeling events that occur with the cardiometabolic syndrome. The MINER acronym will serve as an outline, representing: Myocardial and metabolic-hepatopathy, Intimal and islet, Neurovascular, Endothelial, and Renal oxidation-reduction (redox) stress and remodeling.
Related Concept Videos
01:25Cardiomyopathy I: Introduction and Classification
01:30Coronary Artery Disease I: Introduction
01:26Type II Diabetes I: Introduction
01:21Myocarditis I: Introduction
01:24Type II Diabetes II: Pathophysiology
01:26Diabetes Mellitus: Introduction