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The Role of miRNA in Human Diseases
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The Role of miRNA in Human Diseases

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

Deadline for manuscript submissions: 20 April 2025 | Viewed by 1878

Special Issue Editors

Dr. Seungil Ro

E-Mail Website
Guest Editor
1. Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, USA
2. RosVivo Therapeutics, Applied Research Facility, 1664 N. Virginia St., Reno, NV 89557, USA
Interests: therapeutic microRNAs; diabetes; gastrointestinal disorders; obesity; fatty liver disease
Special Issues, Collections and Topics in MDPI journals
Dr. Seeun Ha

E-Mail Website
Guest Editor
Department of Microbiology and Immunology, University of Nevada School of Medicine, Reno, NV 89557, USA
Interests: microRNAs; noncoding RNAs; diabetes; gastrointestinal disorders; obesity; gastrointestinal surgery in mice; COVID-19
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

microRNAs (miRNAs) have emerged as pivotal regulators in human diseases. These small miRNAs bind to specific target mRNAs, resulting in translational repression. miRNAs play an essential role in a variety of physiological and pathological processes, including diabetes and its comorbidities. Abnormal miRNA expression is linked to numerous diseases, making them valuable therapeutic targets and diagnostic markers. Several miRNAs are currently undergoing clinical development. This Special Issue will focus on original studies uncovering new roles of miRNAs in diabetes and its comorbidities, as well as review articles describing recent insights and highlighting research trends studying the crucial role of miRNAs in these diseases. Research topics may include, but are not limited to, the following:

  1. Role of miRNAs in diabetes;
  2. Role of miRNAs in obesity;
  3. Role of miRNAs in fatty liver disease;
  4. Role of miRNAs in gastrointestinal disease.

Dr. Seungil Ro
Dr. Seeun Ha
Guest Editors

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

  • miRNA
  • diabetes
  • obesity
  • fatty liver disease
  • gastrointestinal disease

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Published Papers (2 papers)

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Research

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19 pages, 5111 KiB  
Article
miR-10a/b-5p-NCOR2 Regulates Insulin-Resistant Diabetes in Female Mice
by Se Eun Ha, Rajan Singh, Byungchang Jin, Gain Baek, Brian G. Jorgensen, Hannah Zogg, Sushmita Debnath, Hahn Sung Park, Hayeong Cho, Claudia Marie Watkins, Sumin Cho, Min-Seob Kim, Moon Young Lee, Tae Yang Yu, Jin Woo Jeong and Seungil Ro
Int. J. Mol. Sci. 2024, 25(18), 10147; https://doi.org/10.3390/ijms251810147 - 21 Sep 2024
Viewed by 918
Abstract
Gender and biological sex have distinct impacts on the pathogenesis of type 2 diabetes (T2D). Estrogen deficiency is known to predispose female mice to T2D. In our previous study, we found that a high-fat, high-sucrose diet (HFHSD) induces T2D in male mice through [...] Read more.
Gender and biological sex have distinct impacts on the pathogenesis of type 2 diabetes (T2D). Estrogen deficiency is known to predispose female mice to T2D. In our previous study, we found that a high-fat, high-sucrose diet (HFHSD) induces T2D in male mice through the miR-10b-5p/KLF11/KIT pathway, but not in females, highlighting hormonal disparities in T2D susceptibility. However, the underlying molecular mechanisms of this hormonal protection in females remain elusive. To address this knowledge gap, we utilized ovariectomized, estrogen-deficient female mice, fed them a HFHSD to induce T2D, and investigated the molecular mechanisms involved in estrogen-deficient diabetic female mice, relevant cell lines, and female T2D patients. Initially, female mice fed a HFHSD exhibited a delayed onset of T2D, but ovariectomy-induced estrogen deficiency promptly precipitated T2D without delay. Intriguingly, insulin (INS) was upregulated, while insulin receptor (INSR) and protein kinase B (AKT) were downregulated in these estrogen-deficient diabetic female mice, indicating insulin-resistant T2D. These dysregulations of INS, INSR, and AKT were mediated by a miR-10a/b-5p-NCOR2 axis. Treatment with miR-10a/b-5p effectively alleviated hyperglycemia in estrogen-deficient T2D female mice, while β-estradiol temporarily reduced hyperglycemia. Consistent with the murine findings, plasma samples from female T2D patients exhibited significant reductions in miR-10a/b-5p, estrogen, and INSR, but increased insulin levels. Our findings suggest that estrogen protects against insulin-resistant T2D in females through miR-10a/b-5p/NCOR2 pathway, indicating the potential therapeutic benefits of miR-10a/b-5p restoration in female T2D management. Full article
(This article belongs to the Special Issue The Role of miRNA in Human Diseases)
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Review

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23 pages, 1581 KiB  
Review
The Ambivalent Role of miRNA-21 in Trauma and Acute Organ Injury
by Aileen Ritter, Jiaoyan Han, Santiago Bianconi, Dirk Henrich, Ingo Marzi, Liudmila Leppik and Birte Weber
Int. J. Mol. Sci. 2024, 25(20), 11282; https://doi.org/10.3390/ijms252011282 - 20 Oct 2024
Viewed by 621
Abstract
Since their initial recognition, miRNAs have been the subject of rising scientific interest. Especially in recent years, miRNAs have been recognized to play an important role in the mediation of various diseases, and further, their potential as biomarkers was recognized. Rising attention has [...] Read more.
Since their initial recognition, miRNAs have been the subject of rising scientific interest. Especially in recent years, miRNAs have been recognized to play an important role in the mediation of various diseases, and further, their potential as biomarkers was recognized. Rising attention has also been given to miRNA-21, which has proven to play an ambivalent role as a biomarker. Responding to the demand for biomarkers in the trauma field, the present review summarizes the contrary roles of miRNA-21 in acute organ damage after trauma with a specific focus on the role of miRNA-21 in traumatic brain injury, spinal cord injury, cardiac damage, lung injury, and bone injury. This review is based on a PubMed literature search including the terms “miRNA-21” and “trauma”, “miRNA-21” and “severe injury”, and “miRNA-21” and “acute lung respiratory distress syndrome”. The present summary makes it clear that miRNA-21 has both beneficial and detrimental effects in various acute organ injuries, which precludes its utility as a biomarker but makes it intriguing for mechanistic investigations in the trauma field. Full article
(This article belongs to the Special Issue The Role of miRNA in Human Diseases)
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