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Epigenetics, Exosomes, and MicroRNAs in Metabolic Disorders

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 10357

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Special Issue Editors

Dr. Marcelina Parrizas

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Guest Editor

Laboratori de Diabetis i Obesitat, CIBERDEM, 08036 Barcelona, Spain
Interests: metabolic disorders (particularly type 2 diabetes and obesity); epigenetics; exosomes; microRNAs and tissue crosstalk in the regulation of metabolism
Special Issues, Collections and Topics in MDPI journals

Dr. Carlos Castaño

E-Mail Website
Co-Guest Editor

Laboratori de Diabetis i Obesitat, CIBERDEM, 08036 Barcelona, Spain
Interests: exosomes; metabolism; diabetes; obesity; animal physiology and surgery

Special Issue Information

Dear Colleagues,

Maintenance of metabolic homeostasis requires the coordinated action of many cell types. This organismal-level communication is mediated by a variety of secreted factors that regulate cellular function to optimize nutrient fluxes. However, environmental influences may induce aberrant epigenetic modifications and disturb tissue crosstalk, leading to decompensations in fuel use that ultimately result in insulin resistance, obesity, and overt disease. Exosomes and other small vesicles released by, amongst other things, the adipose tissue, regulate gene expression in other tissues through microRNA (miRNA) transfer, hence modulating inter-organ crosstalk.

This Special Issue aims to highlight the latest research on the role of epigenetic modifications and exosome-mediated tissue crosstalk in the development of metabolic disorders. The topics that we intend to cover include the following:

- epigenetics and metabolism;

- exosomes and exosomal miRNAs in the regulation of metabolism;

- exosomes and exosomal miRNAs as biomarkers for metabolic disorders; and

- use of exosomes and extracellular vesicles as therapeutic agents and vectors for the treatment of metabolic disorders.

Dr. Marcelina Prrizas
Guest Editor
Dr. Carlos Castaño
Co-Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

extracellular vesicles
microRNAs
epigenetic modifications
tissue crosstalk
diabetes
obesity
non-alcoholic fatty liver disease
biomarkers
therapy

Published Papers (3 papers)

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Research

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17 pages, 4534 KiB

Open AccessArticle

Downregulation of miR-122-5p Activates Glycolysis via PKM2 in Kupffer Cells of Rat and Mouse Models of Non-Alcoholic Steatohepatitis

by Yosuke Inomata, Jae-Won Oh, Kohei Taniguchi, Nobuhiko Sugito, Nao Kawaguchi, Fumitoshi Hirokawa, Sang-Woong Lee, Yukihiro Akao, Shinji Takai, Kwang-Pyo Kim and Kazuhisa Uchiyama

Int. J. Mol. Sci. 2022, 23(9), 5230; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23095230 - 07 May 2022

Cited by 13 | Viewed by 2811

Abstract

Non-alcoholic steatohepatitis (NASH) has pathological characteristics similar to those of alcoholic hepatitis, despite the absence of a drinking history. The greatest threat associated with NASH is its progression to cirrhosis and hepatocellular carcinoma. The pathophysiology of NASH is not fully understood to date. In this study, we investigated the pathophysiology of NASH from the perspective of glycolysis and the Warburg effect, with a particular focus on microRNA regulation in liver-specific macrophages, also known as Kupffer cells. We established NASH rat and mouse models and evaluated various parameters including the liver-to-body weight ratio, blood indexes, and histopathology. A quantitative phosphoproteomic analysis of the NASH rat model livers revealed the activation of glycolysis. Western blotting and immunohistochemistry results indicated that the expression of pyruvate kinase muscle 2 (PKM2), a rate-limiting enzyme of glycolysis, was upregulated in the liver tissues of both NASH models. Moreover, increases in PKM2 and p-PKM2 were observed in the early phase of NASH. These observations were partially induced by the downregulation of microRNA122-5p (miR-122-5p) and occurred particularly in the Kupffer cells. Our results suggest that the activation of glycolysis in Kupffer cells during NASH was partially induced by the upregulation of PKM2 via miR-122-5p suppression. Full article

(This article belongs to the Special Issue Epigenetics, Exosomes, and MicroRNAs in Metabolic Disorders)

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14 pages, 3182 KiB

Open AccessArticle

Postnatal Smoke Exposure Further Increases the Hepatic Nicotine Metabolism in Prenatally Smoke Exposed Male Offspring and Is Linked with Aberrant Cyp2a5 Methylation

by Khosbayar Lkhagvadorj, Zhijun Zeng, Karolin F. Meyer, Laura P. Verweij, Wierd Kooistra, Marjan Reinders-Luinge, Henk W. Dijkhuizen, Inge A. M. de Graaf, Torsten Plösch and Machteld N. Hylkema

Int. J. Mol. Sci. 2021, 22(1), 164; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22010164 - 26 Dec 2020

Cited by 5 | Viewed by 3336

Abstract

Prenatal smoke exposure (PreSE) is a risk factor for nicotine dependence, which is further enhanced by postnatal smoke exposure (PostSE). One susceptibility gene to nicotine dependence is Cytochrome P450 (CYP) 2A6, an enzyme responsible for the conversion of nicotine to cotinine in the liver. Higher CYP2A6 activity is associated with nicotine dependence and could be regulated through DNA methylation. In this study we investigated whether PostSE further impaired PreSE-induced effects on nicotine metabolism, along with Cyp2a5, orthologue of CYP2A6, mRNA expression and DNA methylation. Using a mouse model where prenatally smoke-exposed adult offspring were exposed to cigarette smoke for 3 months, enzyme activity, mRNA levels, and promoter methylation of hepatic Cyp2a5 were evaluated. We found that in male offspring, PostSE increased PreSE-induced cotinine levels and Cyp2a5 mRNA expression. In addition, both PostSE and PreSE changed Cyp2a5 DNA methylation in male groups. PreSE however decreased cotinine levels whereas it had no effect on Cyp2a5 mRNA expression or methylation. These adverse outcomes of PreSE and PostSE were most prominent in males. When considered in the context of the human health aspects, the combined effect of prenatal and adolescent smoke exposure could lead to an accelerated risk for nicotine dependence later in life. Full article

(This article belongs to the Special Issue Epigenetics, Exosomes, and MicroRNAs in Metabolic Disorders)

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Review

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23 pages, 945 KiB

Open AccessReview

Recent Highlights of Research on miRNAs as Early Potential Biomarkers for Cardiovascular Complications of Type 2 Diabetes Mellitus

by Agnieszka Bielska, Magdalena Niemira and Adam Kretowski

Int. J. Mol. Sci. 2021, 22(6), 3153; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22063153 - 19 Mar 2021

Cited by 15 | Viewed by 3445

Abstract

Type 2 diabetes mellitus (T2DM) and its complications pose a serious threat to the life and health of patients around the world. The most dangerous complications of this disease are vascular complications. Microvascular complications of T2DM include retinopathy, nephropathy, and neuropathy. In turn, macrovascular complications include coronary artery disease, peripheral artery disease, and cerebrovascular disease. The currently used diagnostic methods do not ensure detection of the disease at an early stage, and they also do not predict the risk of developing specific complications. MicroRNAs (miRNAs) are small, endogenous, noncoding molecules that are involved in key processes, such as cell proliferation, differentiation, and apoptosis. Recent research has assigned them an important role as potential biomarkers for detecting complications related to diabetes. We suggest that utilizing miRNAs can be a routine approach for early diagnosis and prognosis of diseases and may enable the development of better therapeutic approaches. In this paper, we conduct a review of the latest reports demonstrating the usefulness of miRNAs as biomarkers in the vascular complications of T2DM. Full article

(This article belongs to the Special Issue Epigenetics, Exosomes, and MicroRNAs in Metabolic Disorders)

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