Local inflammatory responses take their toll on the heart

Jager, Saskia C.A. de; Hoefer, Imo E.

doi:10.1016/j.ijcard.2019.07.055

Cited by 2 publications

(1 citation statement)

References 10 publications

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“…TLRs are a major reaction pathway of the inflammatory response after myocardial infarction. Recognition receptors are expressed by inflammatory cells and recognize the danger signal released by injured cells (Jager and Hoefer, 2019;Sircana et al, 2019;Yang M.Y. et al, 2019).…”

Section: Inflammatory Cell Infiltration and Inflammatory Responsementioning

confidence: 99%

Cardioprotective Role of Melatonin in Acute Myocardial Infarction

Jiao

Wang

et al. 2020

Front. Physiol.

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Melatonin is a pleiotropic, indole secreted, and synthesized by the human pineal gland. Melatonin has biological effects including anti-apoptosis, protecting mitochondria, anti-oxidation, anti-inflammation, and stimulating target cells to secrete cytokines. Its protective effect on cardiomyocytes in acute myocardial infarction (AMI) has caused widespread interest in the actions of this molecule. The effects of melatonin against oxidative stress, promoting autophagic repair of cells, regulating immune and inflammatory responses, enhancing mitochondrial function, and relieving endoplasmic reticulum stress, play crucial roles in protecting cardiomyocytes from infarction. Mitochondrial apoptosis and dysfunction are common occurrence in cardiomyocyte injury after myocardial infarction. This review focuses on the targets of melatonin in protecting cardiomyocytes in AMI, the main molecular signaling pathways that melatonin influences in its endogenous protective role in myocardial infarction, and the developmental prospect of melatonin in myocardial infarction treatment.

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Section: Inflammatory Cell Infiltration and Inflammatory Responsementioning

confidence: 99%

Cardioprotective Role of Melatonin in Acute Myocardial Infarction

Jiao

Wang

et al. 2020

Front. Physiol.

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Macrophage Polarization in Atherosclerosis

Eshghjoo

Kim

Jayaraman

et al. 2022

Genes

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The implication of the heterogeneous spectrum of pro- and anti-inflammatory macrophages (Macs) has been an important area of investigation over the last decade. The polarization of Macs alters their functional phenotype in response to their surrounding microenvironment. Macs are the major immune cells implicated in the pathogenesis of atherosclerosis. A hallmark pathology of atherosclerosis is the accumulation of pro-inflammatory M1-like macrophages in coronary arteries induced by pro-atherogenic stimuli; these M1-like pro-inflammatory macrophages are incapable of digesting lipids, thus resulting in foam cell formation in the atherosclerotic plaques. Recent findings suggest that the progression and stability of atherosclerotic plaques are dependent on the quantity of infiltrated Macs, the polarization state of the Macs, and the ratios of different types of Mac populations. The polarization of Macs is defined by signature markers on the cell surface, as well as by factors in intracellular and intranuclear compartments. At the same time, pro- and anti-inflammatory polarized Macs also exhibit different gene expression patterns, with differential cellular characteristics in oxidative phosphorylation and glycolysis. Macs are reflective of different metabolic states and various types of diseases. In this review, we discuss the major differences between M1-like Macs and M2-like Macs, their associated metabolic pathways, and their roles in atherosclerosis.

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Local inflammatory responses take their toll on the heart

Cited by 2 publications

References 10 publications

Cardioprotective Role of Melatonin in Acute Myocardial Infarction

Cardioprotective Role of Melatonin in Acute Myocardial Infarction

Macrophage Polarization in Atherosclerosis

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