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Obesity cardiomyopathy: evidence, mechanisms, and therapeutic implications.

Authors
  • Ren, Jun1, 2
  • Wu, Ne N1
  • Wang, Shuyi3, 4
  • Sowers, James R5
  • Zhang, Yingmei1
  • 1 Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital Fudan University, Shanghai, China. , (China)
  • 2 Department of Laboratory Medicine and Pathology, University of Washington, Seattle, Washington.
  • 3 School of Medicine, Shanghai University, Shanghai, China. , (China)
  • 4 University of Wyoming College of Health Sciences, Laramie, Wyoming.
  • 5 Dalton Cardiovascular Research Center, Diabetes and Cardiovascular Research Center, University of Missouri-Columbia, Columbia, Missouri.
Type
Published Article
Journal
Physiological Reviews
Publisher
American Physiological Society
Publication Date
Oct 01, 2021
Volume
101
Issue
4
Pages
1745–1807
Identifiers
DOI: 10.1152/physrev.00030.2020
PMID: 33949876
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The prevalence of heart failure is on the rise and imposes a major health threat, in part, due to the rapidly increased prevalence of overweight and obesity. To this point, epidemiological, clinical, and experimental evidence supports the existence of a unique disease entity termed "obesity cardiomyopathy," which develops independent of hypertension, coronary heart disease, and other heart diseases. Our contemporary review evaluates the evidence for this pathological condition, examines putative responsible mechanisms, and discusses therapeutic options for this disorder. Clinical findings have consolidated the presence of left ventricular dysfunction in obesity. Experimental investigations have uncovered pathophysiological changes in myocardial structure and function in genetically predisposed and diet-induced obesity. Indeed, contemporary evidence consolidates a wide array of cellular and molecular mechanisms underlying the etiology of obesity cardiomyopathy including adipose tissue dysfunction, systemic inflammation, metabolic disturbances (insulin resistance, abnormal glucose transport, spillover of free fatty acids, lipotoxicity, and amino acid derangement), altered intracellular especially mitochondrial Ca2+ homeostasis, oxidative stress, autophagy/mitophagy defect, myocardial fibrosis, dampened coronary flow reserve, coronary microvascular disease (microangiopathy), and endothelial impairment. Given the important role of obesity in the increased risk of heart failure, especially that with preserved systolic function and the recent rises in COVID-19-associated cardiovascular mortality, this review should provide compelling evidence for the presence of obesity cardiomyopathy, independent of various comorbid conditions, underlying mechanisms, and offer new insights into potential therapeutic approaches (pharmacological and lifestyle modification) for the clinical management of obesity cardiomyopathy.

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