Macrophage roles following myocardial infarction

Lambert, Jessica M.; Lopez, Elizabeth F.; Lindsey, Merry L.

doi:10.1016/j.ijcard.2008.04.059

Cited by 303 publications

(281 citation statements)

References 165 publications

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“…originate from circulating blood monocytes, which are derived from CD34+ bone marrow progenitors [20]. The conversion of monocytes into macrophages begins with their adhesion to the vessel wall.…”

Section: Macrophage Infiltration-macrophagesmentioning

confidence: 99%

Matrix Metalloproteinases: Drug Targets for Myocardial Infarction

Yabluchanskiy¹,

Li²,

Chilton³

et al. 2013

CDT

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Myocardial infarction (MI) remains a major cause of morbidity and mortality worldwide. Rapid advances in the treatment of acute MI have significantly improved short-term outcomes in patient, due in large part to successes in preventing myocardial cell death and limiting infarct area during the time of ischemia and subsequent reperfusion. Matrix metalloproteases (MMPs) play key roles in post-MI cardiac remodeling and in the development of adverse outcomes. This review highlights the importance of MMPs in the injury and remodeling response of the left ventricle and also discusses their potential as therapeutic targets Additional pre-clinical and clinical research is needed to further investigate and understand the cardioprotective effects of MMPs inhibitors.

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Section: Macrophage Infiltration-macrophagesmentioning

confidence: 99%

Matrix Metalloproteinases: Drug Targets for Myocardial Infarction

Yabluchanskiy¹,

Li²,

Chilton³

et al. 2013

CDT

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“…Following MI, resident and recruited macrophages remove necrotic and apoptotic cells, secrete cytokines, and modulate angiogenesis at the infarct site (1). As such, the macrophage is a primary responder cell involved in the regulation of post-MI infarct wound healing at multiple levels (2). According to recent studies, different subsets of macrophages are responsible for these different activities; during the early inflammatory phase (phase 1), proinflammatory macrophages dominate the injury site and phagocytose apoptotic/necrotic myocytes and other debris, whereas during inflammation resolution (phase 2), the dominant subsets are the reparative macrophages, which propagate infarct repair (3,4).…”

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confidence: 99%

Modulation of cardiac macrophages by phosphatidylserine-presenting liposomes improves infarct repair

Harel-Adar

Mordechai

Amsalem

et al. 2011

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

313

255

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Herein we investigated a new strategy for the modulation of cardiac macrophages to a reparative state, at a predetermined time after myocardial infarction (MI), in aim to promote resolution of inflammation and elicit infarct repair. The strategy employed intravenous injections of phosphatidylserine (PS)-presenting liposomes, mimicking the anti-inflammatory effects of apoptotic cells. Following PS-liposome uptake by macrophages in vitro and in vivo, the cells secreted high levels of anti-inflammatory cytokines [transforming growth factor β (TGFβ) and interleukin 10 (IL-10)] and upregulated the expression of the mannose receptor-CD206, concomitant with downregulation of proinflammatory markers, such as tumor necrosis factor α (TNFα) and the surface marker CD86. In a rat model of acute MI, targeting of PS-presenting liposomes to infarct macrophages after injection via the femoral vein was demonstrated by magnetic resonance imaging (MRI). The treatment promoted angiogenesis, the preservation of small scars, and prevented ventricular dilatation and remodeling. This strategy represents a unique and accessible approach for myocardial infarct repair.

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“…Previous studies have demonstrated that AMI elicits inflammatory and innate immune responses, generates oxidative stress/reactive oxygen species (ROS), and initiates the complement cascade 26,[33][34][35] which, in turn, would damage the remote myocardium. 26) In the current study, even at day 90 after AIM, the inflammatory response/oxidative stress at the gene level (MMP-9), cellular level (CD40+ cells), and protein level (oxidized protein) were substantially increased in MI animals compared with those in normal controls.…”

Section: Bmdmsc Transplantation Improved Heart Function -Role Of Immumentioning

confidence: 99%

“…Our findings were comparable to those of previous studies. 26,[33][34][35] Of importance is that these parameters were markedly reduced in MI animals with BMDMSC treatment. Conversely, the gene expression of IL-10, an anti-inflammatory/ immune modulator, was remarkably higher in MI animals with BMDMSC therapy than in those without.…”

Section: Bmdmsc Transplantation Improved Heart Function -Role Of Immumentioning

confidence: 99%

Prompt Bone Marrow-Derived Mesenchymal Stem Cell Therapy Enables Early Porcine Heart Function Recovery from Acute Myocardial Infarction

Fan

Leu²,

Sheu

et al. 2014

Int. Heart J.

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SummaryImpact of early bone marrow-derived mesenchymal stem cell (BMDMSC) implantation on left ventricular (LV) function after AMI was studied.Twelve mini-pigs were equally divided into placebo (AMI through left coronary artery ligation) and cell-treated groups [BMDMSCs (3.0 × 10 7 ) implanted into infarct area (IA)] with myocardium harvested by post-AMI day 90. Six healthy animals served as controls.On post-AMI day 90, magnetic resonance imaging showed a lower LV ejection fraction but higher LV dimensions in the placebo group (P < 0.003) that also had increased IAs but reduced wall thickness (P < 0.005). Pro-apoptotic gene expressions (Bax, caspase-3) and apoptotic nucleus number in IAs and peri-IAs were highest in the placebo group (P < 0.001). Inflammatory biomarker expressions (MMP-9, oxidized protein, CD40+ cells) were highest, whereas those of angiogenesis (VEGF, CD31+ cells, SDF-1α, CXCR4) and myocardium-preservation (connexin43, troponin-I, cytochrome-C) were lowest in the placebo group (P < 0.01).BMDMSC implantation preserved LV function and alleviated remodeling at post-AMI day 90. ( 6-9) Indeed, some studies have reported that SC therapy exhibited only temporary 5,8,9) or minimal 10) effectiveness, or was even ineffective [11][12][13][14][15][16] in improving global LV ejection fraction (LVEF) in patients after acute myocardial infarction (AMI). Further analysis of these clinical trials revealed that stem cell therapy was performed only several days after 5,8,9,[11][12][13] rather than immediately after AMI. Thus, interpretation of the results of these experimental and clinical investigations are difficult because of multiple variables, including the differences in experimental and trial design, cell type used, timing of cell delivery, and parameters for outcome assessment. [1][2][3][4][5][6][7][8][9][10][11][12][13]17) To date, although there is still no definite explanation to account for the discrepancy in findings in the literature, [1][2][3][4][5][6][7][8][9][10][11][12][13] it is rational to believe that two factors are crucial in the success of SC therapy in improving ischemia-related LV dysfunction based on the results of previous reports, 4,5,[7][8][9][10][11][12][13] in other words, a larger number of SCs to be implanted 5,11,18) and an early timing of implantation [19][20][21] in the ischemic zone after AMI. Although small animals are frequently utilized in AMI experimentation From the

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Macrophage roles following myocardial infarction

Cited by 303 publications

References 165 publications

Matrix Metalloproteinases: Drug Targets for Myocardial Infarction

Matrix Metalloproteinases: Drug Targets for Myocardial Infarction

Modulation of cardiac macrophages by phosphatidylserine-presenting liposomes improves infarct repair

Prompt Bone Marrow-Derived Mesenchymal Stem Cell Therapy Enables Early Porcine Heart Function Recovery from Acute Myocardial Infarction

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