Cellular recruitment in myocardial ischaemia/reperfusion injury

Bonaventura, Aldo; Montecucco, Fabrizio; Dallegri, Franco

doi:10.1111/eci.12633

Cited by 88 publications

(70 citation statements)

References 127 publications

(160 reference statements)

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“…Inflammatory processes in ischemic heart disease involve intense chemokine signaling from the forming of the atherosclerotic plaque and plaque destabilization to all phases of acute coronary events and infarct healing (36). IFN-γ inducible chemokines CXCL9, CXCL10, and CXCL11 attract activated T cells through CXCR3 receptor to the site of infarction.…”

Section: Discussionmentioning

confidence: 99%

“…Meanwhile, CXCL4 and CXCL11 promoted the differentiation of T cells into Treg1 cells, responsible for restraining the inflammatory response through IL-10, TGF-β and contact dependent pathways (22, 35, 36). Platelet surface expression of CXCR4 and CXCR7 receptors is elevated in acute coronary syndrome compared to stable angina.…”

Section: Cxcr3 Binding Chemokines In Myocardial Infarctionmentioning

confidence: 99%

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The Role of CXCR3 and Associated Chemokines in the Development of Atherosclerosis and During Myocardial Infarction

et al. 2018

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The chemokine receptor CXCR3 and associated CXC chemokines have been extensively investigated in several inflammatory and autoimmune diseases as well as in tumor development. Recent studies have indicated the role of these chemokines also in cardiovascular diseases. We aimed to present current knowledge regarding the role of CXCR3-binding chemokines in the pathogenesis of atherosclerosis and during acute myocardial infarction.

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Section: Discussionmentioning

confidence: 99%

Section: Cxcr3 Binding Chemokines In Myocardial Infarctionmentioning

confidence: 99%

The Role of CXCR3 and Associated Chemokines in the Development of Atherosclerosis and During Myocardial Infarction

et al. 2018

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“…Similarly, neutrophils recruitment into the injured cardiac tissue is observed during early reperfusion, occurring after myocardial ischaemia. Such inflammatory reaction is required to clear the wound tissue from dead cells and debris, whereas the regulation of neutrophils response is very important to elicit following processes of cardiac recovery and repair …”

Section: Introductionmentioning

confidence: 99%

Neutrophil‐to‐lymphocyte ratio and its relation with pro‐inflammatory mediators, visceral adiposity and carotid intima‐media thickness in population with obesity

Suárez‐Cuenca

Ruíz-Hernández

Mendoza‐Castañeda

et al. 2019

Eur J Clin Investigation

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Background Atherosclerosis represents a cardiovascular risk. Chronic inflammation is a key factor for atherogenic progression. Neutrophil‐to‐lymphocyte ratio (NLR) has been proposed as a novel biomarker for cardiovascular risks. We aimed to explore whether NLR was related to surrogate pro‐atherogenic promoters driving atherogenic progression, as measured by carotid intima‐media thickness (CIMT). Study Design Thirty‐one patients with obesity candidates for bariatric surgery were recruited from Centro Médico Nacional “20 de Noviembre”, ISSSTE, Mexico City. The results are part of the “CROP” study (NCT03561987). NLR was calculated from routine complete blood count, and its relation with plasma pro‐inflammatory mediators (hsCRP, TNF‐α and IL‐1β), adipokines (adiponectin and leptin), adiposity markers (visceral adipose tissue [VAT] determined from CT scan image and VAT individual adipocyte area at histological sample) and CIMT were determined. Results Neutrophil‐to‐lymphocyte ratio correlated with hsCRP (Spearman's r = 0.70 [95% CI 0.46 to 0.85], P < 0.01), TNF‐α (r = 0.69 [0.44 to 0.84], P < 0.0001) and adiponectin (r = −0.69 [−0.84 to −0.45], P < 0.03), as well as with VAT individual adipocyte area (r = 0.64 [0.37 to 0.81], P < 0.0001) and with VAT area (r = 0.43; [0.07 to 0.68], P < 0.01). Leptin and adiponectin showed further independent association with higher NLR (multivariate regression analysis OR 7.9 [95% CI 1.1 to 56.2] P = 0.03 and 0.1 [0.01 to 1.0] P = 0.05, respectively). Moreover, NLR distribution significantly varied between subgroups divided according to progressive CIMT (P = 0.05); whereas adiponectin and VAT adipocyte area associated with CIMT > 0.9 mm (univariate analysis OR 0.1 [0.01 to 1.0] P = 0.05 and 13.1 [1.4 to 126.3] P = 0.03, respectively). Conclusion Neutrophil‐to‐lymphocyte ratio was related to pro‐inflammatory, adiposity biomarkers and progressive subclinical atherogenesis.

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“…Pericytes (Bonaventura, Montecucco, & Dallegri, 2016;Jennings, 2013) Ischemia-induced contraction of microvessels with the aggravation of the capillary no-reflow phenomenon (in the brain) Resolution of inflammation and stabilization of the scar (in the heart)…”

mentioning

confidence: 99%

An overview of protective strategies against ischemia/reperfusion injury: The role of hyperbaric oxygen preconditioning

et al. 2018

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IntroductionIschemia/reperfusion (I/R) injury, such as myocardial infarction, stroke, and peripheral vascular disease, has been recognized as the most frequent causes of devastating disorders and death currently. Protective effect of various preconditioning stimuli, including hyperbaric oxygen (HBO), has been proposed in the management of I/R.MethodsIn this study, we searched and reviewed up‐to‐date published papers to explore the pathophysiology of I/R injury and to understand the mechanisms underlying the protective effect of HBO as conditioning strategy.ResultsAnimal study and clinic observation support the notion that HBO therapy and conditioning provide beneficial effect against the deleterious effects of postischemic reperfusion. Several explanations have been proposed. The first likely mechanism may be that HBO counteracts hypoxia and reduces I/R injury by improving oxygen delivery to an area with diminished blood flow. Secondly, by reducing hypoxia–ischemia, HBO reduces all the pathological events as a consequence of hypoxia, including tissue edema, increased affective area permeability, postischemia derangement of tissue metabolism, and inflammation. Thirdly, HBO may directly affect cell apoptosis, signal transduction, and gene expression in those that are sensitive to oxygen or hypoxia. HBO provides a reservoir of oxygen at cellular level not only carried by blood, but also by diffusion from the interstitial tissue where it reaches high concentration that may last for several hours, improves endothelial function and rheology, and decreases local inflammation and edema.ConclusionEvidence suggests the benefits of HBO when used as a preconditioning stimulus in the setting of I/R injury. Translating the beneficial effects of HBO into current practice requires, as for the “conditioning strategies”, a thorough consideration of risk factors, comorbidities, and comedications that could interfere with HBO‐related protection.

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Cellular recruitment in myocardial ischaemia/reperfusion injury

Cited by 88 publications

References 127 publications

The Role of CXCR3 and Associated Chemokines in the Development of Atherosclerosis and During Myocardial Infarction

The Role of CXCR3 and Associated Chemokines in the Development of Atherosclerosis and During Myocardial Infarction

Neutrophil‐to‐lymphocyte ratio and its relation with pro‐inflammatory mediators, visceral adiposity and carotid intima‐media thickness in population with obesity

An overview of protective strategies against ischemia/reperfusion injury: The role of hyperbaric oxygen preconditioning

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