MicroRNAs as Regulators of Insulin Signaling: Research Updates and Potential Therapeutic Perspectives in Type 2 Diabetes

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Term Occurence Count Dictionary
glucose intolerance 2 endocrinologydiseases
metabolic syndrome 2 endocrinologydiseases
obesity 5 endocrinologydiseases
Insulin 20 endocrinologydiseasesdrugs
diabetes mellitus 2 endocrinologydiseases
diabetic retinopathy 2 endocrinologydiseases

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Insulin 77 Title: International Journal of Molecular SciencesMicroRNAs as Regulators of Insulin Signaling: Research Updates and Potential Therapeutic Perspectives in Type 2 DiabetesLaura NigiGiuseppina
Insulin 2333 prospective therapies involving miRNAs as potential targets for future drugs in T2D.1. Introduction Insulin resistance is a crucial feature and risk factor for Type 2 diabetes (T2D). Namely, it is defined as
Insulin 3238 (e.g., brain), which contribute to molecular and biochemical consequences of insulin resistance [[5]]. Insulin resistance is caused by several factors including obesity, inflammation, endoplasmic reticulum stress,
Insulin 3456 mitochondrial dysfunction. These factors differently contribute to the disruption of insulin signaling. Insulin signaling is a tightly regulated pathway involved in the control of metabolic, pro-survival, and developmental
Insulin 4896 regulation of insulin signal transduction components and their alterations in T2D.2. Molecular Basis of Insulin and Insulin-Like Growth Factor I (IGF-1) SignalingInsulin Receptor (INSR) downstream molecular signaling,
Insulin 4908 insulin signal transduction components and their alterations in T2D.2. Molecular Basis of Insulin and Insulin -Like Growth Factor I (IGF-1) SignalingInsulin Receptor (INSR) downstream molecular signaling, is tightly
Insulin 4954 alterations in T2D.2. Molecular Basis of Insulin and Insulin-Like Growth Factor I (IGF-1) Signaling Insulin Receptor (INSR) downstream molecular signaling, is tightly regulated by a large number of factors and
Insulin 5175 which contribute to a stringent control of energy homeostasis in peripheral insulin target tissues. Insulin signal transduction starts with its binding to INSR. It is a heterotetrameric tyrosine kinase receptor
Insulin 6209 SH2B2/APS, GRB10, GRB14 and/or GRB2. The best characterized scaffold molecules are those belonging to the Insulin Receptor Substrate (IRS) family, which bind INSR through their NH2-terminal pleckstrin homology (PH)
Insulin 10354 skeletal muscle of type 2 diabetic patients and negatively correlated to whole-body insulin action [[35]]. Insulin resistance and diabetes have also been observed as a result of GLUT4 mutations or ablation. Heterozygous
Insulin 11242 mechanisms triggered by insulin in target tissues, include some intermediate molecules which are shared by Insulin -like growth factor-I (IGF-1) signaling as well. IGF-1 has significant structural homology with insulin
Insulin 19672 whose altered expression has been detected in insulin resistance and in T2D.5. MiRNAs as Rheostats of Insulin and IGF-1SignalingThe first report describing a role for miRNAs in the regulation of glucose homeostasis
Insulin 21603 sensitivity and/or proliferation/differentiation cues through the modulation of IGF-1 signaling as well.5.1. Insulin Receptor (INSR)A recent report demonstrated the direct interaction of miR-424-5p with INSR mRNA 3′UTR
Insulin 27192 signaling impairment due to low levels of phosphorylation at specific tyrosine residues [[90]].5.3. Insulin Receptor Substrates (IRS)The best characterized molecules downstream of the INSR, upon its cytoplasmic
Insulin 42659 of insulin signaling, linking insulin resistance, inflammation and cytokine signaling [[135]].5.6. Insulin -Like Growth Factor-1 (IGF-1) and Insulin-Like Growth Factor-1 Receptor (IGF-1R)The regulation of IGF-1
Insulin 42700 resistance, inflammation and cytokine signaling [[135]].5.6. Insulin-Like Growth Factor-1 (IGF-1) and Insulin -Like Growth Factor-1 Receptor (IGF-1R)The regulation of IGF-1 expression and secretion as well as the
Insulin 47876 MAPK/ERK1/2 as extensively reviewed here by others [[148]].6. Extracellular miRNAs as Regulators of Insulin SensitivityTwo breakthrough studies have recently shown how circulating exosomal miRNAs released into
Insulin 57532 ameliorating insulin-resistance and other pathogenic factors contributing to T2D.Figure 1Expression of Insulin /IGF signaling components is modulated by miRNAs. Insulin Receptor (INSR) and Insulin-like Growth Factor
Insulin 57589 contributing to T2D.Figure 1Expression of Insulin/IGF signaling components is modulated by miRNAs. Insulin Receptor (INSR) and Insulin-like Growth Factor (IGF) receptors are preferentially located into plasma
Insulin 57617 1Expression of Insulin/IGF signaling components is modulated by miRNAs. Insulin Receptor (INSR) and Insulin -like Growth Factor (IGF) receptors are preferentially located into plasma membrane macrostructures (caveolae)
Select Disease Character Offset Disease Term Instance
diabetes mellitus 19105 they might represent potential biomarkers for prediction and monitoring of several diseases including diabetes mellitus [[76]].Given the complex scenario in the regulation of gene expression by miRNAs, it is clear that they
diabetes mellitus 23335 found increased in skeletal muscle biopsies obtained from offspring of women affected by gestational diabetes mellitus (GDM) vs. offspring from non-diabetic women during pregnancy. As a matter of fact, GDM women offspring
diabetic retinopathy 30582 proliferation; specifically, miR-126a was found downregulated in retinal endothelial cells from a mouse model of diabetic retinopathy and contributed, through IRS1 modulation, to dysfunctional angiogenesis [[101]].MicroRNA miR-126 has
diabetic retinopathy 43332 Another important miRNA involved in IGF-1 signaling is miR-126, which is downregulated in proliferative diabetic retinopathy and involved in neovascularization. This condition is mediated by several angiogenic factors such as
glucose intolerance 8571 insulin-stimulated glucose uptake [[17],[18],[19]]; similarly, liver specific Irs1 ablation leads to a marked glucose intolerance [[20]]. As a matter of fact, as demonstrated by Hribal ML and colleagues, G792R polymorphism of IRS1,
glucose intolerance 9564 insulin signaling [[25],[26],[27],[28],[29]].Hepatic deletion of Akt1 and Akt2 isoforms resulted into glucose intolerance , insulin resistance and a defective insulin transcription in response to feeding [[30]]. Furthermore,
metabolic syndrome 45977 elucidated in a recent report showing the differential expression of miR-143-3p in serum of patients with metabolic syndrome . Indeed, this miRNAs was found significantly hyperexpressed in serum of these patients as well as in
metabolic syndrome 46438 target IGF-2R receptor and IGFBP5 thus potentially contributing to insulin resistance observed during metabolic syndrome [[145]].Since IGF signaling pathway has been addressed as highly involved in cancer cells growth, some
obesity 2886 pancreatic β-cells [[3]]. It is relevant to mention that growing evidence suggests a relation between obesity , T2D, and brain disturbances [[4]]. Indeed, the defects of insulin signaling in classical peripheral
obesity 3296 consequences of insulin resistance [[5]].Insulin resistance is caused by several factors including obesity , inflammation, endoplasmic reticulum stress, and mitochondrial dysfunction. These factors differently
obesity 8960 Additionally, as demonstrated by several studies [[3],[22],[23]], systemic Irs2 knockout mouse models showed obesity and reduced insulin sensitivity, leading to impaired glucose tolerance and T2D; these results underline
obesity 34478 another study, a miRNA expression profile analysis in visceral adipose tissue from a rodent model of obesity and from obese subjects revealed a decreased expression of miR-26b. This miRNA was reported to target
obesity 55828 differentiation), miR-103 and miR-107 (related to lipid metabolism) as well as of miR-221 and miR-222 (altered in obesity ) was analyzed in retroperitoneal adipose tissue of mice fed with a standard or with a high fat diet

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