Monocytes and macrophages in cardiac injury and repair

Sager, Hendrik B.; Kessler, Thorsten; Schunkert, Heribert

doi:10.21037/jtd.2016.11.17

Cited by 58 publications

(44 citation statements)

References 49 publications

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“…To identify the putative source of this fast increase in the level of miR-320a, we examined its expression in PBMCs since these cells have been implicated in the early inflammatory process (as reviewed elsewhere [10]). Our data indicated that miR-320a was significantly increased in PBMCs of the patients suffering from STEMI at admission before revascularization compared to the controls.…”

Section: Discussionmentioning

confidence: 99%

“…More specifically, peripheral blood mononuclear cells (PBMCs), mainly monocytes, participate in the acute response to heart damage. These cell populations egress from the bone marrow to the blood and infiltrate the myocardium hours after AMI [9,10]. Different studies have suggested that an exacerbated and prolonged inflammatory reaction causes irreparable damage which could be responsible for the progression of LVAR [11,12].…”

Section: Introductionmentioning

confidence: 99%

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Circulating miR-320a as a Predictive Biomarker for Left Ventricular Remodelling in STEMI Patients Undergoing Primary Percutaneous Coronary Intervention

Galeano-Otero

Guisado

Díaz

et al. 2020

JCM

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Restoration of epicardial coronary blood flow, achieved by early reperfusion with primary percutaneous coronary intervention (PPCI), is the guideline recommended to treat patients with ST-segment-elevation myocardial infarction (STEMI). However, despite successful blood restoration, increasing numbers of patients develop left ventricular adverse remodelling (LVAR) and heart failure. Therefore, reliable prognostic biomarkers for LVAR in STEMI are urgently needed. Our aim was to investigate the role of circulating microRNAs (miRNAs) and their association with LVAR in STEMI patients following the PPCI procedure. We analysed the expression of circulating miRNAs in blood samples of 56 patients collected at admission and after revascularization (at 3, 6, 12 and 24 h). The associations between miRNAs and left ventricular end diastolic volumes at 6 months were estimated to detect LVAR. miRNAs were also analysed in samples isolated from peripheral blood mononuclear cells (PBMCs) and human myocardium of failing hearts. Kinetic analysis of miRNAs showed a fast time-dependent increase in miR-133a, miR-133b, miR-193b, miR-499, and miR-320a in STEMI patients compared to controls. Moreover, the expression of miR-29a, miR-29b, miR-324, miR-208, miR-423, miR-522, and miR-545 was differentially expressed even before PPCI in STEMI. Furthermore, the increase in circulating miR-320a and the decrease in its expression in PBMCs were significantly associated with LVAR and correlated with the expression of miR-320a in human failing myocardium from ischaemic origin. In conclusion, we determined the time course expression of new circulating miRNAs in patients with STEMI treated with PPCI and we showed that miR-320a was positively associated with LVAR.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Circulating miR-320a as a Predictive Biomarker for Left Ventricular Remodelling in STEMI Patients Undergoing Primary Percutaneous Coronary Intervention

Galeano-Otero

Guisado

Díaz

et al. 2020

JCM

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“…Later these macrophages, in the reparative phase, undergo transformation and exert profibrotic functions by activating collagen production and neovascularization. A timely resolution of each phase is crucial because spontaneous, prolonged inflammation and fibrosis may be detrimental and determine whether progression to heart failure or repair of cardiac tissue occurs (86). The milieu of progressive atherosclerotic lesions increases the synthesis of leukotriene (LT)B 4 driven by 5-LOX (79,80).…”

Section: Maresins Role In the Clearance Of Atherosclerotic Inflammationmentioning

confidence: 99%

Unified nexus of macrophages and maresins in cardiac reparative mechanisms

Jadapalli

Halade

2018

FASEB j.

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Macrophages are immune-sensing "big eater" phagocytic cells responsible for an innate, adaptive, and regenerative response. After myocardial infarction, macrophages predominantly clear the deceased cardiomyocyte apoptotic or necrotic neutrophils to develop a regenerative and reparative program with the activation of the lipoxygenase-mediated maresin (MaR) metabolome at the site of ischemic injury. The specialized proresolving molecule and macrophage mediator in resolving inflammation, MaR-1, produced by human macrophages, has potent defining effects that limit polymorphonuclear neutrophil infiltration, enhance uptake of apoptotic PMNs, regulate inflammation resolution and tissue regeneration, and reduce pain. In addition to proresolving and anti-inflammatory actions, MaR-1 displays potent tissue regenerative effects in stroke and is an antinociceptive. Macrophages actively participate in the biosynthesis of bioactive MaR-2, which exhibits anti-inflammatory, proresolving, and atherosclerotic effects. A new class of macrophage-derived molecules, MaR conjugates in tissue regeneration, is identified that regulates phagocytosis and the repair and regeneration of damaged tissue. The presented review provides a current summary of the effect of MaR in resolution pathophysiology, with relevance to a cardiac repair program.-Jadapalli, J. K., Halade, G. V. Unified nexus of macrophages and maresins in cardiac reparative mechanisms.

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“…Acute myocardial infarction (AMI), due to a blockage of blood supply to the heart, restricts the availability to oxygen and nutrients, ultimately leading to cell death . Although a fine‐tuned inflammatory response is essential for an efficient cardiac repair following injury, its abnormal intensification can be detrimental and it has been implicated in the pathological remodelling of the heart, namely in AMI and heart failure …”

Section: Introductionmentioning

confidence: 99%

“…1,2 Although a fine-tuned inflammatory response is essential for an efficient cardiac repair following injury, its abnormal intensification can be detrimental and it has been implicated in the pathological remodelling of the heart, namely in AMI and heart failure. 3 It is acknowledged that a highly regulated intercellular communication network between cardiomyocytes, endothelial cells, fibroblasts and immune cells is vital to mount an adequate and efficient response during ischaemic wound healing. 2,4,5 Accordingly, the release of pro-inflammatory cytokines following cardiomyocyte death triggers the recruitment of leukocytes to the damaged sites.…”

Section: Introductionmentioning

confidence: 99%

Ischaemia alters the effects of cardiomyocyte‐derived extracellular vesicles on macrophage activation

Paiva

Martins‐Marques

Jesus

et al. 2018

J Cellular Molecular Medi

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Myocardial ischaemia is associated with an exacerbated inflammatory response, as well as with a deregulation of intercellular communication systems. Macrophages have been implicated in the maintenance of heart homeostasis and in the progression and resolution of the ischaemic injury. Nevertheless, the mechanisms underlying the crosstalk between cardiomyocytes and macrophages remain largely underexplored. Extracellular vesicles (EVs) have emerged as key players of cell‐cell communication in cardiac health and disease. Hence, the main objective of this study was to characterize the impact of cardiomyocyte‐derived EVs upon macrophage activation. Results obtained demonstrate that EVs released by H9c2 cells induced a pro‐inflammatory profile in macrophages, via p38MAPK activation and increased expression of iNOS, IL‐1β and IL‐6, being these effects less pronounced with ischaemic EVs. EVs derived from neonatal cardiomyocytes, maintained either in control or ischaemia, induced a similar pattern of p38MAPK activation, expression of iNOS, IL‐1β, IL‐6, IL‐10 and TNFα. Importantly, adhesion of macrophages to fibronectin was enhanced by EVs released by cardiomyocytes under ischaemia, whereas phagocytic capacity and adhesion to cardiomyocytes were higher in macrophages incubated with control EVs. Additionally, serum‐circulating EVs isolated from human controls or acute myocardial infarction patients induce macrophage activation.According to our model, in basal conditions, cardiomyocyte‐derived EVs maintain a macrophage profile that ensure heart homeostasis, whereas during ischaemia, this crosstalk is affected, likely impacting healing and post‐infarction remodelling.

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Monocytes and macrophages in cardiac injury and repair

Cited by 58 publications

References 49 publications

Circulating miR-320a as a Predictive Biomarker for Left Ventricular Remodelling in STEMI Patients Undergoing Primary Percutaneous Coronary Intervention

Circulating miR-320a as a Predictive Biomarker for Left Ventricular Remodelling in STEMI Patients Undergoing Primary Percutaneous Coronary Intervention

Unified nexus of macrophages and maresins in cardiac reparative mechanisms

Ischaemia alters the effects of cardiomyocyte‐derived extracellular vesicles on macrophage activation

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