A meta-analysis of proinflammatory cytokines in chronic heart failure

Liu, Mao; Chen, Jian; Huang, Dan; Ke, Jianting; Wu, Wei

doi:10.1136/heartasia-2013-010484

Cited by 27 publications

(27 citation statements)

References 35 publications

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“…In contrast, TNF-α deficiency was associated with attenuation of cardiac inflammation and amelioration of adverse left ventricular remodeling and dysfunction in mice subjected to transverse aortic constriction ( Sun et al, 2007 ). Consistent with findings from animal studies implicating TNF-α in the pathogenesis of heart failure, circulating levels of TNF-α have consistently been shown to be elevated in patients with chronic heart failure ( Liu et al, 2014 ).…”

Section: Inflammatory Mediators: Chemokines and Cytokinessupporting

confidence: 53%

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Inflammatory Mediators Drive Adverse Right Ventricular Remodeling and Dysfunction and Serve as Potential Biomarkers

et al. 2018

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Adverse right ventricular (RV) remodeling leads to ventricular dysfunction and failure that represents an important determinant of outcome in patients with pulmonary hypertension (PH). Recent evidence indicates that inflammatory activation contributes to the pathogenesis of adverse RV remodeling and dysfunction. It has been shown that accumulation of inflammatory cells such as macrophages and mast cells in the right ventricle is associated with maladaptive RV remodeling. In addition, inhibition of inflammation in animal models of RV failure ameliorated RV structural and functional impairment. Furthermore, a number of circulating inflammatory mediators have been demonstrated to be associated with RV performance. This work reviews the role of inflammation in RV remodeling and dysfunction and discusses anti-inflammatory strategies that may attenuate adverse structural alterations while promoting improvement of RV function.

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Section: Inflammatory Mediators: Chemokines and Cytokinessupporting

confidence: 53%

“…In contrast, genetic deletion of IL-6 ameliorated pressure overload-induced adverse left ventricular remodeling and dysfunction in mice ( Zhao et al, 2016 ). In patients with chronic heart failure, elevated circulating levels of IL-6 have been reported ( Liu et al, 2014 ).…”

Section: Inflammatory Mediators: Chemokines and Cytokinesmentioning

confidence: 99%

Inflammatory Mediators Drive Adverse Right Ventricular Remodeling and Dysfunction and Serve as Potential Biomarkers

et al. 2018

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“…Previous studies identified elevated proinflammatory cytokines in the brain in mice with chronic heart failure which was associated with increased microglial activation and impaired cognitive performance [26]. Patients in chronic heart failure also exhibit higher levels of proinflammatory cytokines including TNF-α, IL-6, IL-1β, and C-reactive protein [33]. Inflammatory cytokines are known to cross the blood-brain barrier [34].…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-converting enzyme inhibitor treatment early after myocardial infarction attenuates acute cardiac and neuroinflammation without effect on chronic neuroinflammation

Borchert

Hess

Lukacevic

et al. 2020

Eur J Nucl Med Mol Imaging

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Purpose Myocardial infarction (MI) triggers a local inflammatory response which orchestrates cardiac repair and contributes to concurrent neuroinflammation. Angiotensin-converting enzyme (ACE) inhibitor therapy not only attenuates cardiac remodeling by interfering with the neurohumoral system, but also influences acute leukocyte mobilization from hematopoietic reservoirs. Here, we seek to dissect the anti-inflammatory and anti-remodeling contributions of ACE inhibitors to the benefit of heart and brain outcomes after MI. Methods C57BL/6 mice underwent permanent coronary artery ligation (n = 41) or sham surgery (n = 9). Subgroups received ACE inhibitor enalapril (20 mg/kg, oral) either early (anti-inflammatory strategy; 10 days treatment beginning 3 days prior to surgery; n = 9) or delayed (anti-remodeling; continuous from 7 days post-MI; n = 16), or no therapy (n = 16). Cardiac and neuroinflammation were serially investigated using whole-body macrophage-and microglia-targeted translocator protein (TSPO) PET at 3 days, 7 days, and 8 weeks. In vivo PET signal was validated by autoradiography and histopathology. Results Myocardial infarction evoked higher TSPO signal in the infarct region at 3 days and 7 days compared with sham (p < 0.001), with concurrent elevation in brain TSPO signal (+ 18%, p = 0.005). At 8 weeks after MI, remote myocardium TSPO signal was increased, consistent with mitochondrial stress, and corresponding to recurrent neuroinflammation. Early enalapril treatment lowered the acute TSPO signal in the heart and brain by 55% (p < 0.001) and 14% (p = 0.045), respectively. The acute infarct signal predicted late functional outcome (r = 0.418, p = 0.038). Delayed enalapril treatment reduced chronic myocardial TSPO signal, consistent with alleviated mitochondrial stress. Early enalapril therapy tended to lower TSPO signal in the failing myocardium at 8 weeks after MI (p = 0.090) without an effect on chronic neuroinflammation. Conclusions Whole-body TSPO PET identifies myocardial macrophage infiltration and neuroinflammation after MI, and altered cardiomyocyte mitochondrial density in chronic heart failure. Improved chronic cardiac outcome by enalapril treatment derives partially from acute anti-inflammatory activity with complementary benefits in later stages. Whereas early ACE inhibitor therapy lowers acute neuroinflammation, chronic alleviation is not achieved by early or delayed ACE inhibitor therapy, suggesting a more complex mechanism underlying recurrent neuroinflammation in ischemic heart failure.

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“…The release of these pro-inflammatory cytokines promotes atherogenesis by enhancing the release of adhesion molecules, resulting in early monocyte and lymphocyte recruitment in the intima (8). Furthermore, these pro-inflammatory cytokines are considered decisive factors in the pathogenesis and mortality of heart failure (9).…”

Section: Introductionmentioning

confidence: 99%

Anti-inflammatory therapy for cardiovascular disease

Kosmas¹,

Silverio²,

Sourlas³

et al. 2019

Ann. Transl. Med

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Chronic subclinical inflammation is a central process in the pathogenesis of cardiovascular disease (CVD) and it has been linked with both the initiation and progression of atherosclerosis. Several pro-inflammatory cytokines, such as the C-reactive protein (CRP), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) have been described as independent risk factors for coronary heart disease and promoters of atherogenesis. Thus, extensive research is being conducted to assess the role of anti-inflammatory therapy in the primary and secondary prevention of CVD. Our review aims to provide the clinical and scientific data pertaining to the effects of different anti-inflammatory agents administered in patients with CVD.

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A meta-analysis of proinflammatory cytokines in chronic heart failure

Cited by 27 publications

References 35 publications

Inflammatory Mediators Drive Adverse Right Ventricular Remodeling and Dysfunction and Serve as Potential Biomarkers

Inflammatory Mediators Drive Adverse Right Ventricular Remodeling and Dysfunction and Serve as Potential Biomarkers

Angiotensin-converting enzyme inhibitor treatment early after myocardial infarction attenuates acute cardiac and neuroinflammation without effect on chronic neuroinflammation

Anti-inflammatory therapy for cardiovascular disease

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