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Omics Analysis for Personalized Medicine

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 3375

Special Issue Editors


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Guest Editor
1. Department of Pediatrics, Texas Tech University Health Sciences Center, Lubbock, TX, USA
2. KinderGenome Genetics Private Practice, 5347 W Mockingbird, Dallas, TX 75209, USA
Interests: genomics; syndromology; connective tissue dysplasias; Ehlers–Danlos syndrome
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Guest Editor
Institute of Cell Biology, Faculty of Medicine, University of Ljubljana, 1000 Ljubljana, Slovenia
Interests: Establishment and use of in vitro models of interstitial cystitis and other inflammatory diseases; Establishment and use of 3D multi-cellular in vitro models; Studying biomarkers in interstitial cystitis; Studying the anti-inflammatory effect of cannabinoids; Establishment and use of single cell high throughput technologies

Special Issue Information

Dear Colleagues,

Recent advancements in high-throughput sequencing technologies have revolutionized our ability to analyze complex biological samples comprehensively across multiple layers, including genomics, epigenomics, transcriptomics, and proteomics. The integration of these datasets, referred to as multi-omics analysis, enables an unprecedented depth of patient phenotyping based on molecular classification. This approach provides a detailed view of disease mechanisms, enhancing our understanding of complex disorders and paving the way for personalized medicine. This Special Issue focuses on the application of multi-omics approaches in advancing personalized treatment strategies, highlighting the transformative potential of integrating multi-layered data to improve patient care and therapeutic outcomes. Specific attention will be given to immune-mediated diseases, which encompass a diverse spectrum of conditions, ranging from autoimmune to autoinflammatory disorders.

Dr. Golder N. Wilson
Dr. Tadeja Kuret
Guest Editors

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Keywords

  • genomics
  • epigenomics
  • transcriptomics
  • proteomics
  • metabolomics
  • multi-omics
  • high throughput
  • personalized medicine
  • immune-mediated inflammatory diseases

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Published Papers (3 papers)

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Research

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26 pages, 7167 KB  
Article
Transcriptomic Analysis Reveals the Molecular Relationship Between Common Respiratory Infections and Parkinson’s Disease
by Abdulaziz Albeshri, Ahmed Bahieldin and Hani Mohammed Ali
Curr. Issues Mol. Biol. 2025, 47(9), 727; https://doi.org/10.3390/cimb47090727 - 7 Sep 2025
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Abstract
Parkinson’s disease (PD) is one of the most rapidly growing neurological disorders globally. The molecular relationship between common respiratory infections (RIs) and idiopathic Parkinson’s disease (iPD) remains a controversial issue. Multiple studies have linked acute respiratory infections to PD, but the molecular mechanism [...] Read more.
Parkinson’s disease (PD) is one of the most rapidly growing neurological disorders globally. The molecular relationship between common respiratory infections (RIs) and idiopathic Parkinson’s disease (iPD) remains a controversial issue. Multiple studies have linked acute respiratory infections to PD, but the molecular mechanism behind this connection is not significantly defined. Therefore, the aim of our study was to investigate potential molecular interactions between RIs and PD. We retrieved eight publicly available RNA-seq datasets from the NCBI Gene Expression Omnibus (NCBI GEO) and performed extensive bioinformatics analysis, including differential gene expression (DGE) analysis, the identification of overlapped differentially expressed genes (DEGs), weighted gene co-expression network analysis (WGCNA), pathway and functional enrichment analysis, the construction of protein–protein networks, and the identification of hub genes. Additionally, we applied a machine learning method, a Random Forest model (RF), to external RIs datasets to identify the most important genes. We found that ribosomal subunits, mitochondrial complex proteins, proteasome subunits, and proteins encoding ubiquitin are simultaneously downregulated and co-expressed in RIs and PD. Dysregulation of these proteins may disturb multiple pathways, such as those responsible for ribosome biogenesis, protein synthesis, autophagy, and apoptosis; the ubiquitin–proteasome system (UPS); and the mitochondrial respiratory chain. These processes have been implicated in PD’s pathology, namely in the aggregation of α-synuclein, mitochondrial dysfunction, and the death of dopaminergic neuron cells. Our findings suggest that there are significant similarities in transcriptional responses and dysfunctional molecular mechanisms between RIs, PD, and aging. RIs may modulate PD-relevant pathways in an age- or immune-dependent manner; longitudinal studies are needed to examine the RIs risk factor. Therefore, future studies should experimentally investigate the influence of age, vaccination status, infection type, and severity to clarify the role of RIs in PD’s pathogenesis. Full article
(This article belongs to the Special Issue Omics Analysis for Personalized Medicine)
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Review

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25 pages, 1075 KB  
Review
Epigenetic Biomarkers of Cardiovascular Risk in Frail Patients—A Scope Review
by Stanisław Wawrzyniak, Julia Cieśla, Magdalena Woś, Ewa Wołoszyn-Horák, Michał M. Masternak, Tomasz Kukulski, Ewa Stępień and Andrzej Tomasik
Curr. Issues Mol. Biol. 2025, 47(6), 422; https://doi.org/10.3390/cimb47060422 - 5 Jun 2025
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Abstract
Epigenetic biomarkers offer promising potential for early identification and risk stratification of frail individuals susceptible to adverse cardiovascular outcomes. This scope review aimed to identify and evaluate epigenetic biomarkers concurrently associated with frailty and increased cardiovascular risk, potentially facilitating more precise patient stratification [...] Read more.
Epigenetic biomarkers offer promising potential for early identification and risk stratification of frail individuals susceptible to adverse cardiovascular outcomes. This scope review aimed to identify and evaluate epigenetic biomarkers concurrently associated with frailty and increased cardiovascular risk, potentially facilitating more precise patient stratification and treatment decisions. A two-stage literature search was performed using PubMed, Scopus, Web of Science, and Embase databases from the year 2000 through 27 December 2024. Stage 1 identified studies reporting epigenetic biomarkers associated with frailty in blood-derived human samples. Stage 2 assessed cardiovascular relevance by screening the frailty biomarkers identified in Stage 1 for their documented association with cardiovascular diseases. Two independent reviewers conducted screening, data extraction, and risk-of-bias assessments, resolving disagreements via a third reviewer. The primary outcomes were the association of biomarkers with frailty severity and cardiovascular risk. Key epigenetic biomarkers identified included microRNAs (particularly miR-21, miR-146a, miR-451, and miR-92a) and DNA methylation markers (LINE-1 methylation, epigenetic clocks like GrimAge and DunedinPACE, and possibly novel, emerging clocks like DNAmCVDscore and the Smoking Index). Due to specificity limitations, these biomarkers are most promising when used collectively as part of multimarker panels rather than individually. Future research should validate multimarker panels, explore novel biomarkers, and assess clinical integration to optimize precision medicine in frail cardiovascular populations. Full article
(This article belongs to the Special Issue Omics Analysis for Personalized Medicine)
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34 pages, 2285 KB  
Review
How “Omics” Studies Contribute to a Better Understanding of Fuchs’ Endothelial Corneal Dystrophy
by Erika Prašnikar and Spela Stunf Pukl
Curr. Issues Mol. Biol. 2025, 47(3), 135; https://doi.org/10.3390/cimb47030135 - 20 Feb 2025
Cited by 1 | Viewed by 1364
Abstract
Fuchs’ endothelial corneal dystrophy (FECD) is a progressive eye disease characterized by accelerated loss of endothelial cells and the development of focal excrescence (guttae) on Descemet’s membrane, resulting in cornea opacity and vision deterioration. The development of FECD is assumed to be due [...] Read more.
Fuchs’ endothelial corneal dystrophy (FECD) is a progressive eye disease characterized by accelerated loss of endothelial cells and the development of focal excrescence (guttae) on Descemet’s membrane, resulting in cornea opacity and vision deterioration. The development of FECD is assumed to be due to the interplay between genetic and environmental factor risks, causing abnormal extracellular-matrix organization, increased oxidative stress, apoptosis and unfolded protein response. However, the molecular knowledge of FECD is limited. The development of genome-wide platforms and bioinformatics approaches has enabled us to identify numerous genetic loci that are associated with FECD. In this review, we gathered genome-wide studies (n = 31) and sorted them according to genomics (n = 9), epigenomics (n = 3), transcriptomics (n = 15), proteomics (n = 3) and metabolomics (n = 1) levels to characterize progress in understanding FECD. We also extracted validated differentially expressed/spliced genes and proteins identified through comparisons of FECD case and control groups. In addition, highlighted loci from each omics layer were combined according to a comparison with similar study groups from original studies for downstream gene-set enrichment analysis, which provided the most significant biological pathways related to extracellular-matrix organization. In the future, multiomics study approaches are needed to increase the sample size and statistical power to identify strong candidate genes for functional studies on animal models and cell lines for better understanding FECD. Full article
(This article belongs to the Special Issue Omics Analysis for Personalized Medicine)
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