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: 31 October 2025 | Viewed by 1868

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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
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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

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Keywords

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

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Published Papers (2 papers)

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24 pages, 6932 KiB  
Article
Circular Nucleic Acids Act as an Oncogenic MicroRNA Sponge to Inhibit Hepatocellular Carcinoma Progression
by Qianyi Zhang, Pengcheng Sun, Guang Hu, Xuanyao Yu, Wen Zhang, Xuan Feng, Lan Yu and Pengfei Zhang
Biomedicines 2025, 13(5), 1171; https://doi.org/10.3390/biomedicines13051171 - 11 May 2025
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Abstract
Background: Aberrant expression of microRNAs in neoplastic lesions may serve as potential personalized therapeutic targets. To inhibit oncogenic microRNAs (oncomiRs) expression and restore tumor suppressor proteins, linear miRNA sponges have been developed, leading to several drugs in clinical trials. Despite their efficacy, chemically [...] Read more.
Background: Aberrant expression of microRNAs in neoplastic lesions may serve as potential personalized therapeutic targets. To inhibit oncogenic microRNAs (oncomiRs) expression and restore tumor suppressor proteins, linear miRNA sponges have been developed, leading to several drugs in clinical trials. Despite their efficacy, chemically synthesized miRNA inhibitors face challenges with sustained inhibition and high production costs, hindering widespread clinical adoption. Additionally, single-stranded circular RNAs (circRNAs) act as miRNA sponges, enhancing protein expression and demonstrating stability and therapeutic potential in cancer treatment. Our approach involves the use of synthetic single-stranded circular nucleic acids, including circDNA and circRNA, to selectively target and inhibit a variety of aberrantly overexpressed oncomiRs in tumors. The objective of this strategy is to restore the expression levels of multiple tumor suppressor factors and to suppress the malignant progression of tumors. Methods: Our methodology comprises a two-step process. First, we identified tumor suppressor genes (TSGs) with abnormally low expression in hepatocellular carcinoma (HCC) tumor cells by transcriptomic analysis and targeted the upstream cancer miRNA clusters of these TSGs. Second, we designed and validated a fully complementary circDNA or circRNA construct, ligated by T4 DNA ligase or T4 RNA ligase, respectively, that specifically targets the sponge oncomiRs both in vitro and in vivo to inhibit the malignant progression of HCC. Results: CircNAs demonstrated superior, long-lasting therapeutic efficacy against HCC compared to inhibitors. Furthermore, we compared the immune effects in vivo of three different nucleic acid adsorption carriers, including commercial miRNA inhibitor, circDNA, and circRNA. We found that the miRNA inhibitor activates a more robust inflammatory response compared to circDNA and circRNA. Conclusions: These findings underscore the substantial therapeutic potential of circDNA in tumorigenesis and provide novel insights for the formulation of personalized treatment plans for malignant tumors, such as HCC. Full article
(This article belongs to the Special Issue MicroRNA and Its Role in Human Health, 2nd Edition)
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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
Cited by 2 | Viewed by 736
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)
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