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Function and Mechanism of Regulatory Non-coding RNAs in Obesity and Related Diseases

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 (15 November 2022) | Viewed by 2745

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Guest Editor
1. Department of Biochemistry, Dongguk University School of Medicine, Gyeongju 38066, Republic of Korea
2. Channelopathy Research Center (CRC), Dongguk University School of Medicine, Ilsan 10326, Republic of Korea
Interests: mechanotransduction; cytoskeleton remodeling; proliferation; differentiation; myogenesis; sarcopenia; insulin resistance; diabetes; metabolism; glucose metabolism; lipid metabolism; metabolic diseases; energy metabolism
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Special Issue Information

Dear Colleagues,

Obesity is a rapidly growing public health problem associated with multiple chronic diseases, including type 2 diabetes, hypertension, dyslipidemia, coronary heart disease, stroke, and various cancers. Accumulating evidence has elucidated the mechanisms, such as the overload of diacylglycerol and ceramide, oxidative stress, inflammation, and mitochondrial dysfunction, involved in obesity-related diseases. However, the precise mechanisms for how obesity is linked to the pathophysiology of the above diseases are still largely unknown.

In the past decade, regulatory non-coding RNAs, such as miRNAs, siRNAs, piRNAs, and lncRNAs, have become hot issues of current molecular and cellular biology as “key modulators” in physiological processes and pathophysiological processes. They can perform cell-to-cell communication and mediate cellular processes in various ways by regulating gene expression at the epigenetic, transcriptional, post-transcriptional, translational, and post-translational levels. Thus, dysregulation of non-coding RNAs results in the progression of cancers, metabolic diseases, and other complex disorders. However, despite advances in the knowledge of obesity-related diseases and non-coding RNAs, the regulation, function, and mechanism of non-coding RNAs linked to the pathogenesis of obesity-related diseases remain elusive.

This Special Issue will focus on research in discovering the function and mechanism of the regulatory non-coding RNAs in the background of obesity and the pathophysiology of obesity-related diseases. This Issue will also explore new insights into the discovery and potential application of non-coding RNAs as novel biomarkers and therapeutic targets for these diseases. We invite researchers to contribute, either with original research or review articles focusing on every aspect regarding non-coding RNAs associated with obesity and obesity-related diseases.

Prof. Dr. Wan Lee
Guest Editor

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Published Papers (1 paper)

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Research

14 pages, 3362 KiB  
Article
Palmitic Acid-Induced miR-429-3p Impairs Myoblast Differentiation by Downregulating CFL2
by Mai Thi Nguyen, Kyung-Ho Min and Wan Lee
Int. J. Mol. Sci. 2021, 22(20), 10972; https://doi.org/10.3390/ijms222010972 - 11 Oct 2021
Cited by 6 | Viewed by 2232
Abstract
MicroRNAs are known to play a critical role in skeletal myogenesis and maintenance, and cofilin-2 (CFL2) is necessary for actin cytoskeleton dynamics and myogenic differentiation. Nonetheless, target molecules and the modes of action of miRNAs, especially those responsible for the inhibitory mechanism on [...] Read more.
MicroRNAs are known to play a critical role in skeletal myogenesis and maintenance, and cofilin-2 (CFL2) is necessary for actin cytoskeleton dynamics and myogenic differentiation. Nonetheless, target molecules and the modes of action of miRNAs, especially those responsible for the inhibitory mechanism on the myogenesis by saturated fatty acids (SFA) or obesity, still remain unclear. Here, we reported the role played by miR-429-3p on CFL2 expression, actin filament dynamics, myoblast proliferation, and myogenic differentiation in C2C12 cells. Palmitic acid (PA), the most abundant SFA in diet, inhibited the myogenic differentiation of myoblasts, accompanied by CFL2 reduction and miR-429-3p induction. Interestingly, miR-429-3p suppressed the expression of CFL2 by targeting the 3′UTR of CFL2 mRNA directly. Transfection of miR-429-3p mimic in myoblasts increased F-actin formation and augmented nuclear YAP level, thereby promoting cell cycle progression and myoblast proliferation. Moreover, miR-429-3p mimic drastically suppressed the expressions of myogenic factors, such as MyoD, MyoG, and MyHC, and impaired myogenic differentiation of C2C12 cells. Therefore, this study unveiled the crucial role of miR-429-3p in myogenic differentiation through the suppression of CFL2 and provided implications of SFA-induced miRNA in the regulation of actin dynamics and skeletal myogenesis. Full article
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