Editorial (Thematic Issue: Measuring Myocyte Oxidative Stress and Targeting Cytokines to Evaluate Inflammatory Response and Cardiac Repair after Myocardial Infarction)

2015 ◽  
Vol 13 (1) ◽  
pp. 3-5 ◽  
Author(s):  
Vittorio MD
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Inflammatory Response ◽  
Cardiac Repair ◽  
Thematic Issue

scholarly journals Tolerogenic dendritic cells induced by atorvastatin via inhibition of the TLR-4/NF-κB pathway improve cardiac remodeling after myocardial infarction

2020 ◽  
Author(s):  
Jianbing Zhu ◽  
Hang Chen ◽  
Yuanji Ma ◽  
Haibo Liu ◽  
Zhaoyang Chen
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Dendritic Cells ◽  
Inflammatory Response ◽  
Infarct Size ◽  
Inflammatory Reaction ◽  
Ventricular Remodeling ◽  
Inflammatory Responses ◽  
Systolic Function ◽  
Left Ventricular

Abstract BackgroundNecrosis of ischemic cardiomyocytes after myocardial infarction (MI) activates an intense inflammatory reaction. Dendritic cells (DCs) play a crucial role in the repair process after MI. Tolerogenic DCs (tDCs) can inhibit inflammatory responses. Methods and resultsWe investigated the role of atorvastatin and supernatants of necrotic cardiomyocytes (SNC) on DCs. We found that SNC induced DCs maturation, activated TLR-4/NF-κB pathway, promoted inflammatory cytokines secretion and oxidative stress. Co-treatment with SNC and atorvastatin suppressed DC maturation and inflammatory response, which meant that atorvastatin induced DCs tolerate to SNC. Then, we investigated the effect of mDCs induced by SNC and tDCs induced by atorvastatin on ventricular remodeling after MI. tDCs treatment significantly improved the left ventricular systolic function, reduced the infiltration of MPO+ neutrophil, Mac3+ macrophages and CD3+ T cells, inhibited myocardial apoptosis and fibrosis, and decreased infarct size. Compared with PBS, treatment with mDCs did not showed beneficial effect on ventricular remodeling and inflammatory reaction after MI in mice.ConclusionAtorvastatin inactivated the TLR-4/NF-κB pathway, repressed the oxidative stress, inflammatory response, and immune maturity induced by SNC. Treatment with tDCs, induced by co-treated with atorvastatin, preserved left ventricular function, limited infarct size, suppressed the infiltration of inflammatory cells, and attenuated the severity of fibrosis, and reduced the number of apoptotic cardiomyocytes.

scholarly journals Targeted anti–IL-1β platelet microparticles for cardiac detoxing and repair

2020 ◽  
Vol 6 (6) ◽  
pp. eaay0589 ◽  
Author(s):  
Zhenhua Li ◽  
Shiqi Hu ◽  
Ke Huang ◽  
Teng Su ◽  
Jhon Cores ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Side Effects ◽  
Inflammatory Response ◽  
Cardiac Remodeling ◽  
Caspase 3 ◽  
Cardiac Repair ◽  
Promising Strategy ◽  
Heart Injury ◽  
Platelet Microparticles

An acute myocardial infarction (AMI) induces a sterile inflammatory response that facilitates further heart injury and promotes adverse cardiac remodeling. Interleukin-1β (IL-1β) plays a central role in the sterile inflammatory response that results from AMI. Thus, IL-1β blockage is a promising strategy for treatment of AMI. However, conventional IL-1β blockers lack targeting specificity. This increases the risk of serious side effects. To address this problem herein, we fabricated platelet microparticles (PMs) armed with anti–IL-1β antibodies to neutralize IL-1β after AMI and to prevent adverse cardiac remodeling. Our results indicate that the infarct-targeting PMs could bind to the injured heart, increasing the number of anti–IL-1β antibodies therein. The anti–IL-1β platelet PMs (IL1-PMs) protect the cardiomyocytes from apoptosis by neutralizing IL-1β and decreasing IL-1β–driven caspase-3 activity. Our findings indicate that IL1-PM is a promising cardiac detoxification agent that removes cytotoxic IL-1β during AMI and induces therapeutic cardiac repair.

scholarly journals Role of β-Adrenergic Receptors and Estrogen in Cardiac Repair after Myocardial Infarction: An Overview

2021 ◽  
Vol 22 (16) ◽  
pp. 8957
Author(s):  
Paola Matarrese ◽  
Sonia Maccari ◽  
Rosa Vona ◽  
Lucrezia Gambardella ◽  
Tonino Stati ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Inflammatory Response ◽  
Adrenergic Receptors ◽  
Wound Repair ◽  
Active Role ◽  
Cardiac Repair ◽  
Structure Changes ◽  
Β Adrenergic Receptors

Acute myocardial infarction (MI) is associated with an intense inflammatory response that is critical for cardiac repair but is also involved in the pathogenesis of adverse cardiac remodeling, i.e., the set of size, geometry, and structure changes that represent the structural substrate for the development of post-MI heart failure. Deciphering the pathophysiological mechanisms underlying cardiac repair after MI is, therefore, critical to favorably regulate cardiac wound repair and to prevent development of heart failure. Catecholamines and estrogen play an active role in regulating the inflammatory response in the infarcted area. For example, stress-induced catecholamines alter recruitment and trafficking of leukocytes to the heart. Additionally, estrogen affects rate of cardiac rupture during the acute phase of MI, as well as infarct size and survival in animal models of MI. In this review, we will summarize the role of β-adrenergic receptors and estrogen in cardiac repair after infarction in preclinical studies.

Abstract 1526: Presence of Chronic Kidney Disease is Associated with Enhanced Inflammatory Response, Oxidative Stress and Adverse Left Ventricular Remodeling after Reperfused Acute Myocardial Infarction

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Kotaro Naito ◽  
Toshihisa Anzai ◽  
Tsutomu Yoshikawa ◽  
Hidehiro Kaneko ◽  
Yusuke Jo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Clinical Outcome ◽  
Inflammatory Response ◽  
Cardiac Death ◽  
Left Ventricular ◽  
Lv Remodeling

Background: Patients with chronic kidney disease (CKD) have worse clinical outcome after acute myocardial infarction (AMI). We sought to determine the prognostic significance of CKD in patients with reperfused AMI in relation to left ventricular (LV) remodeling. Methods: We examined 120 consecutive patients with reperfused first anterior AMI, admitted within 24 hours of the onset. Glomerular filtration rate (GFR) was estimated by MDRD equation using serum creatinine level on admission. Patients with hemodialysis were excluded. Patients were divided into 2 groups according to the presence or absence of CKD, defined as GFR < 60 ml/min/1.73m 2 . Serum creatine kinase (CK) and C-reactive protein (CRP) levels were serially measured (q. 6, q. 24 hours). Left ventriculography along with plasma interleukin-6 (IL-6) and oxidized low-density lipoprotein (oxLDL) measurements were performed on admission and 2 weeks after AMI. Patients were followed for 27 ± 23 months. Results: Mean GFR was 74 ± 24 ml/min/1.73m 2 and CKD was observed in 25% (n = 30). The prevalence of cardiovascular risk factors, medication and coronary angiographic findings did not differ between the 2 groups. Peak CRP was higher in patients with CKD than those without (p = 0.011), despite similar peak CK. Patients with CKD had higher incidence of in-hospital cardiac death (p = 0.048) and major adverse cardiac events (MACE; p = 0.021), including in- and out-of-hospital cardiac death, non-fatal MI, reintervention, coronary artery bypass grafting and readmission for heart failure, than those without. CKD was associated with greater LV end-diastolic (p = 0.0002) and end-systolic volume (p = 0.0003) and lower LV ejection fraction (p = 0.013) 2 weeks after AMI. Plasma IL-6 (p = 0.037) on admission, and brain natriuretic peptide (p = 0.019) and oxLDL (p = 0.029) 2 weeks after AMI were higher in patients with CKD than in those without. CKD, as well as diabetes mellitus, was an independent predictor of MACE by Cox proportional hazards model analysis (relative risk = 3.13, p = 0.001). Conclusion: CKD was associated with a worse clinical outcome and infarct expansion through modification of inflammatory response and oxidative stress, suggesting an important role of CKD in the development of LV remodeling after reperfused AMI.

Oxidative stress and inflammatory response during and following coronary interventions for acute myocardial infarction

2005 ◽  
Vol 39 (6) ◽  
pp. 629-636 ◽  
Author(s):  
Kirsti Berg ◽  
Per Jynge ◽  
Kristian Bjerve ◽  
Sissel Skarra ◽  
Samar Basu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Inflammatory Response ◽  
Coronary Interventions
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