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MicroRNA and Its Role in Human Health, 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 757

Special Issue Editor


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Guest Editor
Department of Nursing, College of Nursing, Chung Hwa University of Medical Technology Taiwan, Tainan, Taiwan
Interests: rheumatic disease; microRNA expression; microRNA regulation; molecular mechanism; molecular therapy; molecular diagnosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

MicroRNAs (miRs) are fascinating, small, noncoding RNA molecules that play a pivotal role in human health. With an ever-growing body of evidence, miRs have emerged as key players in diagnosing diseases, developing novel therapeutic strategies, and unveiling the intricate molecular mechanisms and signaling pathways that govern various disease processes. miRs function by binding to the 3'-untranslated regions of specific messenger RNAs (mRNAs), leading to their degradation or the suppression of translation. This ability to upregulate or downregulate target genes based on miR expression levels provides a unique window into understanding disease progression and regulation. By exploring miR expression and target gene interactions, we can unlock new avenues for therapeutic interventions.

The regulation of miRs can be harnessed using cutting-edge techniques, including vector-based miR precursors or sponges, agomiR or antagomiR transfer, and genome editing via CRISPR. Additionally, high-throughput miR arrays offer large-scale data that can uncover novel disease associations, expanding our understanding of the roles miRs play in human health.

In this Special Issue, we aim to present a comprehensive collection of studies exploring the diverse roles of miRs across a wide range of disease models. We encourage the submission of original research articles and comprehensive reviews that examine miRs as diagnostic markers, therapeutic agents, or key pathogenic molecules. We are excited to collaborate with you on this cutting-edge exploration of microRNAs and look forward to your valuable contributions to the progression of this dynamic field.

Dr. Shih-Yao Chen
Guest Editor

Manuscript Submission Information

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Keywords

  • microRNA
  • disease models
  • disease associations
  • molecular mechanism
  • molecular diagnosis
  • molecular therapy

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Published Papers (1 paper)

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Research

18 pages, 3855 KiB  
Article
Differential Pattern of Circulating MicroRNA Expression in Patients with Intracranial Atherosclerosis
by Marine M. Tanashyan, Anton A. Raskurazhev, Alla A. Shabalina, Andrey S. Mazur, Vladislav A. Annushkin, Polina I. Kuznetsova, Sergey N. Illarioshkin and Mikhail A. Piradov
Biomedicines 2025, 13(2), 514; https://doi.org/10.3390/biomedicines13020514 - 19 Feb 2025
Viewed by 289
Abstract
Background: Intracranial atherosclerosis (ICAS) is a major cause of ischemic stroke, yet fundamental studies regarding epigenetic regulation of ICAS are lacking. We hypothesized that, due to anatomical and/or functional differences, extracranial atherosclerosis is distinct from ICAS, which may explain the clinical variability as [...] Read more.
Background: Intracranial atherosclerosis (ICAS) is a major cause of ischemic stroke, yet fundamental studies regarding epigenetic regulation of ICAS are lacking. We hypothesized that, due to anatomical and/or functional differences, extracranial atherosclerosis is distinct from ICAS, which may explain the clinical variability as well. Methods: We chose a number of miRNAs involved in various steps of atherogenesis (namely, miR-712/205-5p/-3p, miR-106b-3p/-5p, miR-146a-3p/-5p, miR-100-3p/miR-5p, miR-200c-3p/-5p, miR-532-3p/-5p, and miR-126-3p/-5p) and examined their plasma levels in a cohort of patients with carotid stenosis > 50% (n = 35, mean age: 65 years, 54% male; 12 patients had ICAS). Results: A differential pattern of circulating miR expression was found in ICAS patients: there was an overexpression of miR-712/205-5p, miR-106b-5p, miR-146a-5p, miR-200c-5p, miR-532-3p, and miR-126-3p. The following miRs were underexpressed in intracranial atherosclerosis—miR-712/205-3p and miR-100-3p. These changes represent a plethora of atherogenic mechanisms: smooth muscle cell migration (miR-712/205, miR-532), foam cell formation (miR-106b, miR-146a), endothelial dysfunction (miR-200c), low-density lipoprotein-induced vascular damage (miR-100), and leukocyte recruitment (miR-126). In symptomatic ICAS patients, we observed a statistically significant upregulation of miR-712/205-3p and miR-146a-5p. Conclusions: Overall, the findings of our pilot study revealed several new and interesting associations: (1) intracranial atherosclerosis seems to have a different epigenetic profile (regarding circulating microRNA expression) than isolated extracranial vessel involvement; (2) ischemic stroke in ICAS may be potentiated by other pathophysiologic mechanisms than in extracranial-only atherosclerosis (ECAS). Certain miRs (e.g., miR-712/205) seem to have a larger impact on ICAS than on extracranial atherosclerosis; this may be potentially linked to difference between extra- and intracranial artery morphology and physiology, and/or may lead to the said differences. This underscores the importance of making a distinction in future epigenetic studies between ECAS and ICAS, as the mechanisms of atherogenesis are likely to vary. Full article
(This article belongs to the Special Issue MicroRNA and Its Role in Human Health, 2nd Edition)
Show Figures

Figure 1

Figure 1
<p>Flow-chart of patients included in this study. ICAS—intracranial atherosclerosis, ECAS—extracranial only atherosclerosis, CTA—CT-angiography, MRA—magnetic resonance angiography, HRVWI—high-resolution vessel wall imaging.</p>
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<p>Patient ID#2. MRI signs of intracranial atherosclerosis of the brachiocephalic arteries: uneven stenosis of both internal carotid arteries (ICA) at the intracranial level, with signs of an eccentric pattern of contrast enhancement. MRI in T2 mode with high resolution (T2-HR) in the coronary (<b>a</b>), MRI T1 db f/s, before (<b>b</b>) and after (<b>c</b>) intravenous contrast injection with high-spatial-resolution T1-weighed imaging and suppression of the signal from bloodstream and fat. Red arrows—intracranial atherosclerotic plaque; white arrows—contrast enhancement in the vessel wall.</p>
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<p>Patient ID#1. The MRI data correspond to stenosis of the left internal carotid artery (60–65%) with signs of an eccentric pattern of contrast enhancement. MRI in T2 mode with high resolution (T2-HR) in the coronary plane (<b>a</b>), MRI T1 db f/s, before (<b>b</b>) and after (<b>c</b>) intravenous contrast injection with high-spatial-resolution T1-weighed imaging and suppression of the signal from bloodstream and fat. White arrows—intracranial atherosclerotic plaque.</p>
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<p>Box-plot showing miR expression in symptomatic patients with ICAS (sICAS), ECAS (sECAS), and patients without prior stroke. Shown are only significant pairwise differences (Holm–Bonferroni correction for multiple comparisons, <span class="html-italic">p</span> &lt; 0.05). * <span class="html-italic">p</span> &lt; 0.05; ** <span class="html-italic">p</span> &lt; 0.01; *** <span class="html-italic">p</span> &lt; 0.001.</p>
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<p>Atherosclerosis-related targets of studied miRs. Shown are cross-sections of extra-(<b>left</b>) and intracranial (<b>right</b>) arteries with anatomical features characteristic of each level (i.e., a thicker internal elastic lamina, absence of external elastic lamina and vasa vasorum, and low proportion of elastic fibers in intracranial vessels). LDL—low-density lipoprotein; ox-LDL—oxidized LDL; SMCs—smooth muscle cells; TIMP3—metalloproteinase inhibitor 3; * ox-LDL induced vascular damage.</p>
Full article ">
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