Obesity, Hypertension, and Cardiac Dysfunction

Mouton, Alan J.; Li, Xuan; Hall, Michael E.; Hall, John E.

doi:10.1161/circresaha.119.312321

Cited by 338 publications

(180 citation statements)

References 184 publications

Supporting

Mentioning

172

Contrasting

Unclassified

Order By: Relevance

“…The development of both ventricular dysfunction and mechanoenergetic impairments in diabetes/obesity is clearly multifactorial and complex and, in addition to alterations in myocardial substrate utilization, the involvement of Ca 2+ handling, oxidative stress, mitochondrial dysfunction, and structural remodeling has been proposed. 49 50 65 86 87 88 Diabetes is also associated with impaired myocardial Ca 2+ handling, including increased ryanodine receptor 2 Ca 2+ leak, 88 89 which most likely contributes to the increased oxygen consumption demonstrated herein and in previous studies. 75 79 80 90 91 …”

Section: Changes In Cardiac Metabolism and Function In Obese And Diabsupporting

confidence: 59%

“…Many studies have demonstrated that obesity (isolated or co-existing with hypertension) in humans is associated with abnormal diastolic function, 47 48 49 whereas impairment of systolic function is not consistently observed. 50 Obesity-related dysfunction includes left heart remodeling (i.e., left atrial dilatation and LV hypertrophy) as well as abnormalities in LV contractile and relaxation functions (i.e., LV stiffness and impaired relaxation).…”

Section: Inflammation and Lipid Overload Cause Dysregulation Of Myocamentioning

confidence: 99%

See 1 more Smart Citation

Impact of Obesity-Related Inflammation on Cardiac Metabolism and Function

Larsen

Jansen

2021

J Lipid Atheroscler

View full text Add to dashboard Cite

This review focuses on the role of adipose tissue in obese individuals in the development of metabolic diseases, and their consequences for metabolic and functional derangements in the heart. The general idea is that the expansion of adipocytes during the development of obesity gives rise to unhealthy adipose tissue, characterized by low-grade inflammation and the release of proinflammatory adipokines and fatty acids (FAs). This condition, in turn, causes systemic inflammation and elevated FA concentrations in the circulation, which links obesity to several pathologies, including impaired insulin signaling in cardiac muscle and a subsequent shift in myocardial substrate oxidation in favor of FAs and reduced cardiac efficiency. This review also argues that efforts to prevent obesity-related cardiometabolic disease should focus on anti-obesogenic strategies to restore normal adipose tissue metabolism.

show abstract

Section: Changes In Cardiac Metabolism and Function In Obese And Diabsupporting

confidence: 59%

Section: Inflammation and Lipid Overload Cause Dysregulation Of Myocamentioning

confidence: 99%

Impact of Obesity-Related Inflammation on Cardiac Metabolism and Function

Larsen

Jansen

2021

J Lipid Atheroscler

View full text Add to dashboard Cite

show abstract

“…Both diabetes and hypertension can lead to chronic inflammation and activation of macrophages toward an inflammatory phenotype. Although macrophages play a key role in cardiac remodeling, dysregulation of macrophages between pro-inflammatory and anti-inflammatory phenotypes promotes excessive inflammation and cardiac injury [ 145 ]. Cardiac metabolic reprogramming has been implicated in cardiac adaptation to injury [ 146 , 147 , 148 ], though the healthy heart relies mainly on mitochondrial oxidative phosphorylation metabolism of fatty acid for its energy demands.…”

Section: Role Of Macrophages In Cardiac Remodeling In Hypertensionmentioning

confidence: 99%

“…Macrophage metabolic shifts are not only required for energy demands but also for regulation of pro- and anti-inflammatory processes. Macrophage metabolic shifts are tightly regulated by several intracellular signaling pathways, in which NF-κB, HIF-1α, PDK1 and PPAR-γ play an important role in reprogramming the macrophages [ 145 ]. However, investigation pertaining to cardiac macrophage metabolism is still young and requires thorough investigations.…”

Section: Future Direction Of Cardiac Macrophagesmentioning

confidence: 99%

Role of Cardiac Macrophages on Cardiac Inflammation, Fibrosis and Tissue Repair

Lafuse

Wozniak

Rajaram

2020

Cells

225

175

View full text Add to dashboard Cite

The immune system plays a pivotal role in the initiation, development and resolution of inflammation following insult or damage to organs. The heart is a vital organ which supplies nutrients and oxygen to all parts of the body. Heart failure (HF) has been conventionally described as a disease associated with cardiac tissue damage caused by systemic inflammation, arrhythmia and conduction defects. Cardiac inflammation and subsequent tissue damage is orchestrated by the infiltration and activation of various immune cells including neutrophils, monocytes, macrophages, eosinophils, mast cells, natural killer cells, and T and B cells into the myocardium. After tissue injury, monocytes and tissue-resident macrophages undergo marked phenotypic and functional changes, and function as key regulators of tissue repair, regeneration and fibrosis. Disturbance in resident macrophage functions such as uncontrolled production of inflammatory cytokines, growth factors and inefficient generation of an anti-inflammatory response or unsuccessful communication between macrophages and epithelial and endothelial cells and fibroblasts can lead to aberrant repair, persistent injury, and HF. Therefore, in this review, we discuss the role of cardiac macrophages on cardiac inflammation, tissue repair, regeneration and fibrosis.

show abstract

“…The host reaches a new homeostasis level, but it completely fails in resolution of inflammation. Chronic inflammation underlies many diseases, and studies have shown that dysfunction of neutrophils [ 11 ] and macrophages [ 41 ] play a major role in contributing to chronic inflammation.…”

Section: Inflammation Responsesmentioning

confidence: 99%

Neutrophils and Macrophages as Targets for Development of Nanotherapeutics in Inflammatory Diseases

Gao

Kaur

et al. 2020

Pharmaceutics

View full text Add to dashboard Cite

Neutrophils and macrophages are major components of innate systems, playing central roles in inflammation responses to infections and tissue injury. If they are out of control, inflammation responses can cause the pathogenesis of a wide range of diseases, such as inflammatory disorders and autoimmune diseases. Precisely regulating the functions of neutrophils and macrophages in vivo is a potential strategy to develop immunotherapies to treat inflammatory diseases. Advances in nanotechnology have enabled us to design nanoparticles capable of targeting neutrophils or macrophages in vivo. This review discusses the current status of how nanoparticles specifically target neutrophils or macrophages and how they manipulate leukocyte functions to inhibit their activation for inflammation resolution or to restore their defense ability for pathogen clearance. Finally, we present a novel concept of hijacking leukocytes to deliver nanotherapeutics across the blood vessel barrier. This review highlights the challenges and opportunities in developing nanotherapeutics to target leukocytes for improved treatment of inflammatory diseases.

show abstract

Obesity, Hypertension, and Cardiac Dysfunction

Cited by 338 publications

References 184 publications

Impact of Obesity-Related Inflammation on Cardiac Metabolism and Function

Impact of Obesity-Related Inflammation on Cardiac Metabolism and Function

Role of Cardiac Macrophages on Cardiac Inflammation, Fibrosis and Tissue Repair

Neutrophils and Macrophages as Targets for Development of Nanotherapeutics in Inflammatory Diseases

Contact Info

Product

Resources

About