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Role of MicroRNAs 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: 31 August 2024 | Viewed by 716

Special Issue Editor


E-Mail Website1 Website2
Guest Editor
1. Department of Radiology, Michigan State University, Interdisciplinary Science and Technology Building, East Lansing, MI 48824, USA
2. Precision Health Program, Michigan State University, Interdisciplinary Science and Technology Building, East Lansing, MI 48824, USA
Interests: tissue slide-based microRNA diagnostics; microRNA biology and evolution; cell type-specific activities of microRNAs in oncology with a focus on breast and pancreatic cancer; nanoparticle-based delivery of microRNA activity modulators
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

MicroRNAs are an abundant class of short non-coding RNAs. MicroRNAs regulate gene expression predominantly at the posttranscriptional stage by interacting with partially complementary binding sites on the 3′ UTR of mRNAs of their target genes. Through this mode of regulation and via coordinated interactions with multiple target genes, many miRNAs have been etiologically and mechanistically linked to a variety of human diseases. More than 1900 entries of short non-coding RNA sequences have been registered with miRBase.org for the human genome. Furthermore, 546 of these entries have been curated as bona fide microRNA genes as per mirgenedb.org.

The human miRNome has distinct evolutionary origins; some human microRNAs are conserved in all animals (bilateria), whereas other human microRNAs have more recent origins being specific to eutheria (placental animals), primates, or even restricted to only humans. The evolutionary origin of some miRNAs provides clues of their role in human development, physiology, and pathological processes. Similarly, the tissue- and cell type-specific expression (e.g., muscle cells, neurons, hepatocytes) of some miRNAs offers clues of their biological activity and regulatory networks.

This Special Issue will provide a comprehensive update on the latest findings of human disease–associated miRNAs, with a focus on the clinical application of miRNAs as biomarkers for diagnosis and prognosis, treatment prediction, and miRNA-based therapeutic strategies. Given the broad implication of microRNAs in human diseases, we expect this Special Issue to cover different human diseases from cancer to cardiovascular disease to neurological conditions and degenerative diseases.

We welcome both original research papers and review articles that describe advances in deciphering the etiological and epidemiological links of microRNAs to human diseases, detection methodology and bioinformatics approaches to uncover miRNA signatures, fundamental biology and molecular approaches to determine the mechanistic details of miRNA contribution to human diseases, and diagnostic and therapeutic development to apply this knowledge for the treatment of human diseases in first-in-human clinical trials.

Dr. Lorenzo F. Sempere
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.

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Keywords

  • microRNAs, miRNAs, miRs
  • preclinical models
  • target interaction, regulatory networks
  • oncology, cancer biology
  • cardiovascular disease
  • neurodegenerative conditions
  • diagnostic applications
  • therapeutic development and clinical trials

Published Papers (1 paper)

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Research

24 pages, 6271 KiB  
Article
miRNA Expression Profiles in Isolated Ventricular Cardiomyocytes: Insights into Doxorubicin-Induced Cardiotoxicity
by Yohana Domínguez Romero, Gladis Montoya Ortiz, Susana Novoa Herrán, Jhon Osorio Mendez and Luis A. Gomez Grosso
Int. J. Mol. Sci. 2024, 25(10), 5272; https://doi.org/10.3390/ijms25105272 - 12 May 2024
Viewed by 466
Abstract
Doxorubicin (DOX), widely used as a chemotherapeutic agent for various cancers, is limited in its clinical utility by its cardiotoxic effects. Despite its widespread use, the precise mechanisms underlying DOX-induced cardiotoxicity at the cellular and molecular levels remain unclear, hindering the development of [...] Read more.
Doxorubicin (DOX), widely used as a chemotherapeutic agent for various cancers, is limited in its clinical utility by its cardiotoxic effects. Despite its widespread use, the precise mechanisms underlying DOX-induced cardiotoxicity at the cellular and molecular levels remain unclear, hindering the development of preventive and early detection strategies. To characterize the cytotoxic effects of DOX on isolated ventricular cardiomyocytes, focusing on the expression of specific microRNAs (miRNAs) and their molecular targets associated with endogenous cardioprotective mechanisms such as the ATP-sensitive potassium channel (KATP), Sirtuin 1 (SIRT1), FOXO1, and GSK3β. We isolated Guinea pig ventricular cardiomyocytes by retrograde perfusion and enzymatic dissociation. We assessed cell morphology, Reactive Oxygen Species (ROS) levels, intracellular calcium, and mitochondrial membrane potential using light microscopy and specific probes. We determined the miRNA expression profile using small RNAseq and validated it using stem-loop qRT-PCR. We quantified mRNA levels of some predicted and validated molecular targets using qRT-PCR and analyzed protein expression using Western blot. Exposure to 10 µM DOX resulted in cardiomyocyte shortening, increased ROS and intracellular calcium levels, mitochondrial membrane potential depolarization, and changes in specific miRNA expression. Additionally, we observed the differential expression of KATP subunits (ABCC9, KCNJ8, and KCNJ11), FOXO1, SIRT1, and GSK3β molecules associated with endogenous cardioprotective mechanisms. Supported by miRNA gene regulatory networks and functional enrichment analysis, these findings suggest that DOX-induced cardiotoxicity disrupts biological processes associated with cardioprotective mechanisms. Further research must clarify their specific molecular changes in DOX-induced cardiac dysfunction and investigate their diagnostic biomarkers and therapeutic potential. Full article
(This article belongs to the Special Issue Role of MicroRNAs in Human Diseases)
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