Inflammation in Myocardial Diseases

Marchant, David; Boyd, John H.; Lin, David C.; Granville, David J.; Garmaroudi, Farshid S.; McManus, Bruce M.

doi:10.1161/circresaha.111.243170

Cited by 246 publications

(172 citation statements)

References 211 publications

(227 reference statements)

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“…Inflammatory processes are involved in many conditions that injure the myocardium and cause both structural and functional defects in the heart (15,16), and glucocorticoids have welldocumented anti-inflammatory actions. Examination of the genes dysregulated in the hearts of the cardioGRKO mice by both IPA and GO revealed a prominent association with the immune response and inflammation.…”

Section: Discussionmentioning

confidence: 99%

Essential role of stress hormone signaling in cardiomyocytes for the prevention of heart disease

Oakley

Ren²,

Cruz‐Topete³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

108

115

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Significance Stress is increasingly associated with heart disease. Glucocorticoids are primary stress hormones, yet their direct role in the heart is poorly understood. Mice lacking the glucocorticoid receptor specifically in cardiomyocytes die prematurely from heart failure. The deficiency in glucocorticoid signaling leads to the aberrant regulation of a large cohort of genes strongly associated with both cardiovascular and inflammatory disease processes. These findings reveal an obligate role for cardiomyocyte glucocorticoid receptors in maintaining normal heart function and define a paradigm for stress in cardiovascular disease.

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Section: Discussionmentioning

confidence: 99%

Essential role of stress hormone signaling in cardiomyocytes for the prevention of heart disease

Oakley

Ren²,

Cruz‐Topete³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

108

115

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“…27) Previous investigations have demonstrated that interventions targeted for infl ammatory responses improve MI. 1,2) Among numerous infl ammatory mediators involved, IL-1β is an early and prominent mediator for inflammatory responses in MI.…”

Section: Nlrp3 Inflammasome and Myocardial Infarction (Mi)mentioning

confidence: 99%

NLRP3 Inflammasome as a Novel Player in Myocardial Infarction

2014

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SummaryInfl ammasomes are multiple protein complexes that serve as molecular platforms to activate caspase-1 and regulate maturation of a potent proinfl ammatory cytokine, interleukin (IL)-1β, as well as proinfl ammatory cell death, pyroptosis. Although several types of infl ammasomes have been reported so far, recent investigations indicate that the NLRP3 infl ammasome recognizes non-microbial danger signals and leads to sterile infl ammatory responses in various disease conditions. Sterile infl ammatory responses are also implicated in the development of myocardial infarction (MI). In particular, IL-1β is an early and prominent mediator of infl ammatory responses in MI, suggesting the pathophysiologic role of NLRP3 infl ammasomes in MI. This review highlights the current state of knowledge regarding the role of NLRP3 infl ammasomes in MI. (Int Heart J 2014; 55: 101-105)

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“…It is known that inflammation plays an important role in the pathophysiology of I/R injury 4, 5, 6. Myocardial I/R injury‐induced inflammatory responses are typically associated with increased cytokines secretion, upregulated expression of cell adhesion molecules, and enhanced neutrophil infiltration and microvascular permeability 7.…”

Section: Introductionmentioning

confidence: 99%

Ticagrelor attenuates myocardial ischaemia–reperfusion injury possibly through downregulating galectin‐3 expression in the infarct area of rats

Liu

et al. 2018

Brit J Clinical Pharma

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AimsThe full benefits of myocardial revascularization strategies applied to acute myocardial infarction patients might be reduced by myocardial ischaemia and reperfusion (I/R) injury. It is known that inflammation plays an important role in the pathogenesis of I/R injury and galectin‐3, a known inflammatory factor, is actively involved in ischaemia‐induced inflammation and fibrosis of various organs. Previous studies demonstrated that anti‐platelets therapy with ticagrelor, a new P2Y12 receptor antagonist, could effectively attenuate myocardial I/R injury and I/R injury‐related inflammatory responses. It remains unknown whether the cardioprotective effects of ticagrelor are also mediated by modulating myocardial galectin‐3 expression.MethodsWe determined the ratio of infarct area (IA)/area at risk (AAR), expression of galectin‐3, TNF‐α and IL‐6 in infarct area of rats treated with placebo (equal volume saline per gastric gavage immediately after LAD ligation, then once daily till study end) or ticagrelor (150 mg kg−1 dissolved in saline per gastric gavage immediately after LAD ligation, then once daily till study end) at 24 h, 3 and 7 days post I (45 min)/R injury. Sham‐operated rats served as control.ResultsOur results showed that ticagrelor treatment significantly reduced IA/AAR ratio at 3 and 7 days post I/R, downregulated mRNA and protein expression of galectin‐3, as well as mRNA expression of TNF‐α and IL‐6 in infarct area at 24 h, 3 and 7 days post I/R.ConclusionsOur results suggest that the cardioprotective effects of ticagrelor might partly be mediated by downregulating galectin‐3 expression in infarct area in this rat model of myocardial I/R injury.

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Inflammation in Myocardial Diseases

Cited by 246 publications

References 211 publications

Essential role of stress hormone signaling in cardiomyocytes for the prevention of heart disease

Essential role of stress hormone signaling in cardiomyocytes for the prevention of heart disease

NLRP3 Inflammasome as a Novel Player in Myocardial Infarction

Ticagrelor attenuates myocardial ischaemia–reperfusion injury possibly through downregulating galectin‐3 expression in the infarct area of rats

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