Macrophage MicroRNAs as Therapeutic Targets for Atherosclerosis, Metabolic Syndrome, and Cancer.

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glucose intolerance 2 endocrinologydiseases
hyperlipidemia 2 endocrinologydiseases
metabolic syndrome 8 endocrinologydiseases
obesity 23 endocrinologydiseases

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glucose intolerance 23754 Transplantation of macrophages pretreated with miR-130b inhibitor attenuates adipose tissue inflammation and glucose intolerance in mice fed on an HFD [[91]].3.3. miRNAs Secreted from Adipose Tissue Influence the Distant TissuesThe
glucose intolerance 39783 adipose tissues and the other organs. Upregulation of miR-155 in ATM-Exos induces insulin resistance and glucose intolerance in the liver. Induction of miR-155 expression by hyperlipidemia-associated endotoxemia promotes IL-6
hyperlipidemia 26693 [[105],[106]]. This effect may be mediated by the beneficial role of miR-155 in glucose homeostasis during hyperlipidemia [[105]]. Hyperlipidemia-associated endotoxemia leads to an increase in miR-155 expression in pancreatic
hyperlipidemia 39852 induces insulin resistance and glucose intolerance in the liver. Induction of miR-155 expression by hyperlipidemia -associated endotoxemia promotes IL-6 gene transcription and increases production of Glucagon-like peptide-1
metabolic syndrome 1042 targets in immune disorders. In this review, we will summarize the role of miRNAs in atherosclerosis, metabolic syndrome , and cancer by modulating macrophage phenotypes, which has been supported by in vivo evidence.1. IntroductionThe
metabolic syndrome 1989 central role in pathological process of several diseases, such as atherosclerosis, obesity-induced metabolic syndrome , and cancer. The role of miRNAs in macrophages has been summarized somewhere else [[1],[2]], here we
metabolic syndrome 2224 macrophage-derived miRNAs that have recently come to light as affecting atherogenesis, obesity-induced metabolic syndrome and cancer, which is supported by in vivo evidences.1.1. Macrophage Plasticity and PolarizationMacrophages
metabolic syndrome 21366 expression in ATMs is changed by obesity. However, the role of miR-193 and miR-126 in obesity-induced metabolic syndrome needs to be validated in the animal models.miR-223 is a hematopoietic miRNA and mainly expressed in
metabolic syndrome 23466 whereas miR-34a is globally deleted in [[88]]. Thus, the cell-specific effect of miR-34a on obesity and metabolic syndrome should be further studied in the future.MiR-130b is upregulated in macrophages of HFD-fed mice, which
metabolic syndrome 26071 These studies indicate the pathological role of miR-155 in obesity-induced chronic inflammation and metabolic syndrome .In addition to regulate macrophage phenotypes, miR-155 mediates adipocyte dysfunction caused by inflammatory
metabolic syndrome 37610 aspects of macrophages and thereby affect several immune disorders, like atherosclerosis, obesity-induced metabolic syndrome and cancer. Targeting miRNAs through the application of modified oligonucleotides may become an effective
metabolic syndrome 39377 cholesterol transport. The T bar indicates the inhibitory effect.Figure 2Role of miRNAs in obesity-induced metabolic syndrome by regulating macrophage phenotypes. Obesity upregulates the expression of several miRNAs, like miR-34a
obesity 1973 inflammation plays a central role in pathological process of several diseases, such as atherosclerosis, obesity -induced metabolic syndrome, and cancer. The role of miRNAs in macrophages has been summarized somewhere
obesity 2208 will review macrophage-derived miRNAs that have recently come to light as affecting atherogenesis, obesity -induced metabolic syndrome and cancer, which is supported by in vivo evidences.1.1. Macrophage Plasticity
obesity 19395 including but not limited to type 2 diabetes, cardiovascular diseases and cancer [[74],[75]]. Although once obesity was considered to be a simple lipid-storage disease, the notion that obesity is a chronic inflammatory
obesity 19472 [[74],[75]]. Although once obesity was considered to be a simple lipid-storage disease, the notion that obesity is a chronic inflammatory process has now been accepted broadly [[76]]. Obesity-associated metabolic
obesity 19709 cause of insulin resistance and impaired glucose metabolism [[76]]. The pathophysiological link between obesity , inflammation, and insulin resistance was first demonstrated when the researchers found the secretion
obesity 20412 mice, display the alternatively activated phenotype and support adipose homeostasis [[81]]. During obesity , inflammatory mediators released from adipose tissue, such as saturated fatty acids, cytokines, and
obesity 20912 Macrophage PolarizationLike atherosclerosis, several miRNAs may contribute to the pathological process of obesity -related immunometabolic diseases by regulating macrophage polarization. miR-193 and miR-126 inhibit
obesity 21297 adipocytes from obese men [[84]], although it is not known whether their expression in ATMs is changed by obesity . However, the role of miR-193 and miR-126 in obesity-induced metabolic syndrome needs to be validated
obesity 21350 whether their expression in ATMs is changed by obesity. However, the role of miR-193 and miR-126 in obesity -induced metabolic syndrome needs to be validated in the animal models.miR-223 is a hematopoietic miRNA
obesity 23454 [[90]], whereas miR-34a is globally deleted in [[88]]. Thus, the cell-specific effect of miR-34a on obesity and metabolic syndrome should be further studied in the future.MiR-130b is upregulated in macrophages
obesity 24036 insulin target tissues, pancreatic islets or cardiovascular system result in the causal link between obesity and other immunometabolic disorders, such as diabetes and cardiovascular diseases. There are many substances
obesity 25343 tolerance through regulating liver gene expression by the transferred miRNAs [[99],[100]]. Moreover, obesity induces changes of miRNA expression in ATM-Exos, suggesting the pathological role of these miRNAs in
obesity 25452 induces changes of miRNA expression in ATM-Exos, suggesting the pathological role of these miRNAs in obesity [[98]].In contrast to lean mice, obesity causes upregulation of miR-155 expression in both ADMs and
obesity 25493 ATM-Exos, suggesting the pathological role of these miRNAs in obesity [[98]].In contrast to lean mice, obesity causes upregulation of miR-155 expression in both ADMs and ATM-Exos. By targeting PPARγ, miR-155 mediates
obesity 26030 M2 markers, Arginase-1 and Ym1 [[101]]. These studies indicate the pathological role of miR-155 in obesity -induced chronic inflammation and metabolic syndrome.In addition to regulate macrophage phenotypes, miR-155
obesity 26266 dysfunction caused by inflammatory cytokines (e.g., TNF-α), which may contribute to the diet-induced obesity progression in C57BL/6 mice by limiting brown adipose tissue differentiation [[102],[103],[104]]. By
obesity 26467 [[102],[103],[104]]. By contrast, in hyperlipidemic Ldlr−/− and Apoe−/− mice, miR-155 deficiency aggravates obesity , which is accompanied by augmented gonadal adipocyte hypertrophy and macrophage recruitment in adipose
obesity 27078 Ldlr−/− mice fed on an HFD, elevated plasma GLP-1 levels by miR-155 may limit the progression of obesity and adipose tissue inflammation [[105]]. Accordingly, global transgenic overexpression of miR-155 improves
obesity 27467 of miR-155 in different cell types might be the reason for the controversial effects of miR-155 on obesity , which can be studied by using cell-specific miR-155 knockout mouse model.These studies indicate that
obesity 27782 sensitivity, which might be the result from different kinds of miRNAs packaged in the exosomes. During obesity , the metabolic organs may uptake the exosomes derived from both cell types in the adipose tissue, however,
obesity 37594 roles in many aspects of macrophages and thereby affect several immune disorders, like atherosclerosis, obesity -induced metabolic syndrome and cancer. Targeting miRNAs through the application of modified oligonucleotides
obesity 37980 of miRNAs are highly context- and cell type-dependent, like the controversial effect of miR-155 on obesity -induced diabetes. Unfortunately, the miRNA-regulated context-specific network is still poorly understood,
obesity 39361 reverse cholesterol transport. The T bar indicates the inhibitory effect.Figure 2Role of miRNAs in obesity -induced metabolic syndrome by regulating macrophage phenotypes. Obesity upregulates the expression of

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