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Biomolecules
Special Issues
Posttranscriptional Regulation of Metabolic Disorders
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Posttranscriptional Regulation of Metabolic Disorders

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (15 August 2021) | Viewed by 16677

Special Issue Editor

Dr. Cristina M. Ramírez Hidalgo

E-Mail Website
Guest Editor
IMDEA Research Institute on Food & Health Sciences, 28049 Madrid, Spain
Interests: posttranscriptional regulation; miRNAs; RNA binding proteins; metabolism; diabetes; atherosclerosis

Special Issue Information

Dear Colleagues,

Post-transcriptional regulation of gene expression by microRNAs (miRNAs) and RNA-binding proteins (RBPs) plays a key role in a number of biological functions, and its dysregulation underlies many metabolic diseases that extensively impact public health systems worldwide. A number of studies over the past two decades have revealed the importance of several post-transcriptional regulators in pathophysiological states characterized by aberrant glucose and lipid homeostasis such as diabetes, atherosclerosis, and Alzeimer’s disease. In this Special Issue, we aim to present original research articles and up-to-date reviews of the current understanding of regulatory non-coding RNAs and RBPs and their roles in normal physiology and in metabolic wdisorders, with special emphasis on their potential use as targets for future therapeutics.

We look forward to reading your contributions.

Dr. Cristina M. Ramírez Hidalgo
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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • Metabolic diseases
  • Non-coding RNA
  • RNA binding proteins
  • Alzheimer’s disease
  • Diabetes
  • Atherosclerosis
  • Glucose homeostasis
  • Lipid metabolism
  • Inflammation

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Published Papers (4 papers)

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Research

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15 pages, 2490 KiB  
Article
Regulatory Action of Plasma from Patients with Obesity and Diabetes towards Muscle Cells Differentiation and Bioenergetics Revealed by the C2C12 Cell Model and MicroRNA Analysis
by Natalya V. Khromova, Anton V. Fedorov, Yi Ma, Kirill A. Kondratov, Stanislava S. Prikhodko, Elena V. Ignatieva, Marina S. Artemyeva, Anna D. Anopova, Aleksandr E. Neimark, Anna A. Kostareva, Alina Yu. Babenko and Renata I. Dmitrieva
Biomolecules 2021, 11(6), 769; https://doi.org/10.3390/biom11060769 - 21 May 2021
Cited by 3 | Viewed by 3427
Abstract
Obesity and type 2 diabetes mellitus (T2DM) are often combined and pathologically affect many tissues due to changes in circulating bioactive molecules. In this work, we evaluated the effect of blood plasma from obese (OB) patients or from obese patients comorbid with diabetes [...] Read more.
Obesity and type 2 diabetes mellitus (T2DM) are often combined and pathologically affect many tissues due to changes in circulating bioactive molecules. In this work, we evaluated the effect of blood plasma from obese (OB) patients or from obese patients comorbid with diabetes (OBD) on skeletal muscle function and metabolic state. We employed the mouse myoblasts C2C12 differentiation model to test the regulatory effect of plasma exposure at several levels: (1) cell morphology; (2) functional activity of mitochondria; (3) expression levels of several mitochondria regulators, i.e., Atgl, Pgc1b, and miR-378a-3p. Existing databases were used to computationally predict and analyze mir-378a-3p potential targets. We show that short-term exposure to OB or OBD patients’ plasma is sufficient to affect C2C12 properties. In fact, the expression of genes that regulate skeletal muscle differentiation and growth was downregulated in both OB- and OBD-treated cells, maximal mitochondrial respiration rate was downregulated in the OBD group, while in the OB group, a metabolic switch to glycolysis was detected. These alterations correlated with a decrease in ATGL and Pgc1b expression in the OB group and with an increase of miR-378a-3p levels in the OBD group. Full article
(This article belongs to the Special Issue Posttranscriptional Regulation of Metabolic Disorders)
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16 pages, 3694 KiB  
Article
The Presence of Cholesteryl Ester Transfer Protein (CETP) in Endothelial Cells Generates Vascular Oxidative Stress and Endothelial Dysfunction
by Amarylis C. B. A. Wanschel, Daniele M. Guizoni, Estela Lorza-Gil, Alessandro G. Salerno, Adriene A. Paiva, Gabriel G. Dorighello, Ana Paula Davel, Wayne Balkan, Joshua M. Hare and Helena C. F. Oliveira
Biomolecules 2021, 11(1), 69; https://doi.org/10.3390/biom11010069 - 7 Jan 2021
Cited by 23 | Viewed by 3892
Abstract
Endothelial dysfunction precedes atherosclerosis and is an independent predictor of cardiovascular events. Cholesterol levels and oxidative stress are key contributors to endothelial damage, whereas high levels of plasma high-density lipoproteins (HDL) could prevent it. Cholesteryl ester transfer protein (CETP) is one of the [...] Read more.
Endothelial dysfunction precedes atherosclerosis and is an independent predictor of cardiovascular events. Cholesterol levels and oxidative stress are key contributors to endothelial damage, whereas high levels of plasma high-density lipoproteins (HDL) could prevent it. Cholesteryl ester transfer protein (CETP) is one of the most potent endogenous negative regulators of HDL-cholesterol. However, whether and to what degree CETP expression impacts endothelial function, and the molecular mechanisms underlying the vascular effects of CETP on endothelial cells, have not been addressed. Acetylcholine-induced endothelium-dependent relaxation of aortic rings was impaired in human CETP-expressing transgenic mice, compared to their non-transgenic littermates. However, endothelial nitric oxide synthase (eNOS) activation was enhanced. The generation of superoxide and hydrogen peroxide was increased in aortas from CETP transgenic mice, while silencing CETP in cultured human aortic endothelial cells effectively decreased oxidative stress promoted by all major sources of ROS: mitochondria and NOX2. The endoplasmic reticulum stress markers, known as GADD153, PERK, and ARF6, and unfolded protein response effectors, were also diminished. Silencing CETP reduced endothelial tumor necrosis factor (TNF) α levels, intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) expression, diminishing monocyte adhesion. These results support the notion that CETP expression negatively impacts endothelial cell function, revealing a new mechanism that might contribute to atherosclerosis. Full article
(This article belongs to the Special Issue Posttranscriptional Regulation of Metabolic Disorders)
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Review

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24 pages, 567 KiB  
Review
Posttranscriptional Regulation of Insulin Resistance: Implications for Metabolic Diseases
by Ana Pérez-García, Marta Torrecilla-Parra, Mario Fernández-de Frutos, Yolanda Martín-Martín, Virginia Pardo-Marqués and Cristina M. Ramírez
Biomolecules 2022, 12(2), 208; https://doi.org/10.3390/biom12020208 - 26 Jan 2022
Cited by 24 | Viewed by 5421
Abstract
Insulin resistance defines an impairment in the biologic response to insulin action in target tissues, primarily the liver, muscle, adipose tissue, and brain. Insulin resistance affects physiology in many ways, causing hyperglycemia, hypertension, dyslipidemia, visceral adiposity, hyperinsulinemia, elevated inflammatory markers, and endothelial dysfunction, [...] Read more.
Insulin resistance defines an impairment in the biologic response to insulin action in target tissues, primarily the liver, muscle, adipose tissue, and brain. Insulin resistance affects physiology in many ways, causing hyperglycemia, hypertension, dyslipidemia, visceral adiposity, hyperinsulinemia, elevated inflammatory markers, and endothelial dysfunction, and its persistence leads to the development metabolic disease, including diabetes, obesity, cardiovascular disease, or nonalcoholic fatty liver disease (NAFLD), as well as neurological disorders such as Alzheimer’s disease. In addition to classical transcriptional factors, posttranscriptional control of gene expression exerted by microRNAs and RNA-binding proteins constitutes a new level of regulation with important implications in metabolic homeostasis. In this review, we describe miRNAs and RBPs that control key genes involved in the insulin signaling pathway and related regulatory networks, and their impact on human metabolic diseases at the molecular level, as well as their potential use for diagnosis and future therapeutics. Full article
(This article belongs to the Special Issue Posttranscriptional Regulation of Metabolic Disorders)
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14 pages, 863 KiB  
Review
Regulation of Long Non-Coding RNAs by Statins in Atherosclerosis
by Diamantis I. Tsilimigras, Sofia-Iris Bibli, Gerasimos Siasos, Evangelos Oikonomou, Despina N. Perrea, Konstantinos Filis, Dimitrios Tousoulis and Fragiska Sigala
Biomolecules 2021, 11(5), 623; https://doi.org/10.3390/biom11050623 - 22 Apr 2021
Cited by 7 | Viewed by 3027
Abstract
Despite increased public health awareness, atherosclerosis remains a leading cause of mortality worldwide. Significant variations in response to statin treatment have been noted among different populations suggesting that the efficacy of statins may be altered by both genetic and environmental factors. The existing [...] Read more.
Despite increased public health awareness, atherosclerosis remains a leading cause of mortality worldwide. Significant variations in response to statin treatment have been noted among different populations suggesting that the efficacy of statins may be altered by both genetic and environmental factors. The existing literature suggests that certain long noncoding RNAs (lncRNAs) might be up- or downregulated among patients with atherosclerosis. LncRNA may act on multiple levels (cholesterol homeostasis, vascular inflammation, and plaque destabilization) and exert atheroprotective or atherogenic effects. To date, only a few studies have investigated the interplay between statins and lncRNAs known to be implicated in atherosclerosis. The current review characterizes the role of lncRNAs in atherosclerosis and summarizes the available evidence related to the effect of statins in regulating lncRNAs. Full article
(This article belongs to the Special Issue Posttranscriptional Regulation of Metabolic Disorders)
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