IL33 attenuates ventricular remodeling after myocardial infarction through inducing alternatively activated macrophages ethical standards statement

Li, Jing; Shen, Deliang; Tang, Junnan; Wang, Yunzhe; Wang, Bo; Xiao, Yue; Cao, Chang; Shi, Xiaojing; Liu, Hong‐Min; Zhao, Wen; Zhang, Jinying

doi:10.1016/j.ejphar.2019.04.046

Cited by 20 publications

(6 citation statements)

References 43 publications

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“…Immunofluorescence revealed that SA can increase CD68 + /CD206 + macrophage infiltration by 23%, which suggested that SA can promote the polarization of M2 macrophages. M2 macrophages secrete various antiinflammatory factors and many studies have shown that activation and increase of M2 macrophages can attenuate ventricular remodeling (34)(35)(36)(37). Inhibition or depletion of M2 macrophage inhibiting M2 macrophage activationresulted in deterioration of cardiac function, enlargement of infarct area and increase of inflammatory cell infiltration after MI (38,39).…”

Section: Discussionmentioning

confidence: 99%

Sinapic Acid Attenuated Cardiac Remodeling After Myocardial Infarction by Promoting Macrophage M2 Polarization Through the PPARγ Pathway

Yang

Xiong

Zou

et al. 2022

Front. Cardiovasc. Med.

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BackgroundMacrophage polarization is an important regulatory mechanism of ventricular remodeling. Studies have shown that sinapic acid (SA) exerts an anti-inflammatory effect. However, the effect of SA on macrophages is still unclear.ObjectivesThe purpose of the study was to investigate the role of SA in macrophage polarization and ventricular remodeling after myocardial infarction (MI).MethodsAn MI model was established by ligating the left coronary artery. The rats with MI were treated with SA for 1 or 4 weeks after MI. The effect of SA on bone marrow-derived macrophages (BMDMs) was also observed in vitro.ResultsCardiac systolic dysfunction was significantly improved after SA treatment. SA reduced MCP-1 and CCR2 expression and macrophage infiltration. SA decreased the levels of the inflammatory factors TNF-α, IL-1α, IL-1β, and iNOS and increased the levels of the M2 macrophage markers CD206, Arg-1, IL-10, Ym-1, Fizz-1, and TGF-β at 1 week after MI. SA significantly increased CD68+/CD206+ macrophage infiltration. Myocardial interstitial fibrosis and MMP-2 and MMP-9 levels were decreased, and the sympathetic nerve marker TH and nerve sprouting marker GAP43 were suppressed after SA treatment at 4 weeks after MI. The PPARγ level was notably upregulated after SA treatment. In vitro, SA also increased the expression of PPARγ mRNA in BMDMs and IL-4-treated BMDMs in a concentration-dependent manner. SA enhanced Arg1 and IL-10 expression in BMDMs, and the PPARγ antagonist GW9662 attenuated M2 macrophage marker expression.ConclusionsOur results demonstrated that SA attenuated structural and neural remodeling by promoting macrophage M2 polarization via PPARγ activation after MI.

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Section: Discussionmentioning

confidence: 99%

Sinapic Acid Attenuated Cardiac Remodeling After Myocardial Infarction by Promoting Macrophage M2 Polarization Through the PPARγ Pathway

Yang

Xiong

Zou

et al. 2022

Front. Cardiovasc. Med.

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“…The JAK/STAT in angiogenesis STAT3 plays an important role in the formation of blood vessels, and this process is essential for controlling compensatory hypertrophy and remodeling 394 . Not only that, the JAK/STAT signaling pathway also induces polarization of M2 macrophages, promoting myocardial angiogenesis and myocardial functional reconstruction 356,395 . Specific STAT3 knockout mice displayed no changes in VEGF expression, but these mice exhibited levels of VEGF inhibitors, such as thrombospondin 1 (TSP-1), and increased levels of proteins involved in the formation of interstitial matrix, such as osteopontin (OPN) and plasminogen activator inhibitor-1 (PAI-1) 394 .…”

Section: Jak/stat Signaling Pathway In MImentioning

confidence: 99%

Signaling pathways and targeted therapy for myocardial infarction

Zhang

Wang

et al. 2022

Sig Transduct Target Ther

345

117

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Although the treatment of myocardial infarction (MI) has improved considerably, it is still a worldwide disease with high morbidity and high mortality. Whilst there is still a long way to go for discovering ideal treatments, therapeutic strategies committed to cardioprotection and cardiac repair following cardiac ischemia are emerging. Evidence of pathological characteristics in MI illustrates cell signaling pathways that participate in the survival, proliferation, apoptosis, autophagy of cardiomyocytes, endothelial cells, fibroblasts, monocytes, and stem cells. These signaling pathways include the key players in inflammation response, e.g., NLRP3/caspase-1 and TLR4/MyD88/NF-κB; the crucial mediators in oxidative stress and apoptosis, for instance, Notch, Hippo/YAP, RhoA/ROCK, Nrf2/HO-1, and Sonic hedgehog; the controller of myocardial fibrosis such as TGF-β/SMADs and Wnt/β-catenin; and the main regulator of angiogenesis, PI3K/Akt, MAPK, JAK/STAT, Sonic hedgehog, etc. Since signaling pathways play an important role in administering the process of MI, aiming at targeting these aberrant signaling pathways and improving the pathological manifestations in MI is indispensable and promising. Hence, drug therapy, gene therapy, protein therapy, cell therapy, and exosome therapy have been emerging and are known as novel therapies. In this review, we summarize the therapeutic strategies for MI by regulating these associated pathways, which contribute to inhibiting cardiomyocytes death, attenuating inflammation, enhancing angiogenesis, etc. so as to repair and re-functionalize damaged hearts.

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“…For instance, IL-33 can be released by various cells following necrosis. It not only induces macrophage reprogramming, leading to uncoupling of the mitochondrial respiratory chain and increased production of the mitochondrial-derived metabolite itaconate, thus promoting the resolution of inflammation and initiation of tissue damage repair; but also activates the JAK/STAT signaling pathway to induce M2 macrophage polarization, thereby impeding the progression of cardiac fibrosis and improving cardiac systolic and diastolic function (110,111). Indeed, Liu et al demonstrated that in vitro induced M2 macrophages could be transplanted into hearts of heart failure mice models, confirmed that M2 macrophages can transfer mitochondria to damaged cardiomyocytes, which promote cell survival under stress conditions and alleviate cardiac fibrosis and cardiomyocyte apoptosis (112).…”

Section: Macrophage Phenotype Switching Intimately Linked To Metaboli...mentioning

confidence: 99%

The effect of macrophages and their exosomes in ischemic heart disease

Wang,

Li,

Liu

et al. 2024

Front. Immunol.

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Ischemic heart disease (IHD) is a leading cause of disability and death worldwide, with immune regulation playing a crucial role in its pathogenesis. Various immune cells are involved, and as one of the key immune cells residing in the heart, macrophages play an indispensable role in the inflammatory and reparative processes during cardiac ischemia. Exosomes, extracellular vesicles containing lipids, nucleic acids, proteins, and other bioactive molecules, have emerged as important mediators in the regulatory functions of macrophages and hold promise as a novel therapeutic target for IHD. This review summarizes the regulatory mechanisms of different subsets of macrophages and their secreted exosomes during cardiac ischemia over the past five years. It also discusses the current status of clinical research utilizing macrophages and their exosomes, as well as strategies to enhance their therapeutic efficacy through biotechnology. The aim is to provide valuable insights for the treatment of IHD.

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IL33 attenuates ventricular remodeling after myocardial infarction through inducing alternatively activated macrophages ethical standards statement

Cited by 20 publications

References 43 publications

Sinapic Acid Attenuated Cardiac Remodeling After Myocardial Infarction by Promoting Macrophage M2 Polarization Through the PPARγ Pathway

Sinapic Acid Attenuated Cardiac Remodeling After Myocardial Infarction by Promoting Macrophage M2 Polarization Through the PPARγ Pathway

Signaling pathways and targeted therapy for myocardial infarction

The effect of macrophages and their exosomes in ischemic heart disease

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