Genetic Variations and Human Diseases: From Mechanisms to Translational Medicine

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Genomics and Proteomics".

Deadline for manuscript submissions: 20 January 2027 | Viewed by 203

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Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan
Interests: cancer genomics; translational medical sciences; personalized genomic; pharmaceutical sciences
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Special Issue Information

Dear Colleagues,

Advances in genetic research have profoundly expanded our understanding of disease susceptibility, marking a transformative era for biomedical science and precision medicine. A growing body of evidence has demonstrated that genetic variations, particularly single-nucleotide polymorphisms (SNPs), are closely associated with the risk, progression, and clinical outcomes of a wide spectrum of diseases. These include, but are not limited to, cancers, cardiovascular diseases, neurological and neurodegenerative disorders, metabolic syndromes, autoimmune diseases, inflammatory conditions, and other complex multifactorial diseases.

Such findings highlight the pivotal role of genetic variation in disease pathogenesis, emphasizing its potential not only as a molecular marker for risk stratification and early detection but also as a foundation for mechanism-based therapeutic development and personalized intervention strategies.

Despite substantial progress, inconsistencies across studies remain common. These discrepancies often arise from factors such as population heterogeneity, limited sample sizes, methodological variability, and differences in ethnic and environmental backgrounds. These challenges underscore the pressing need for well-designed, robust, and translational studies to validate existing findings, uncover shared or disease-specific genetic mechanisms, and explore new avenues in genetic medicine.

We invite translational scientists worldwide to submit original research that elucidates the genetic basis of human diseases across all disease categories. Studies should integrate experimental, clinical, or population-based validation; submissions relying solely on in silico or dry-lab analyses will not be considered. By contributing to Life, authors will help bridge genetic discoveries with biological mechanisms and clinical relevance, fostering advances that extend across disease boundaries.

I look forward to receiving your valuable contributions.

Prof. Dr. Da-Tian Bau
Guest Editor

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Keywords

  • biomarkers
  • cancer genomics
  • diagnosis
  • disease susceptibility
  • personalized medicine
  • single nucleotide polymorphism (SNP)

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Published Papers (1 paper)

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Research

17 pages, 711 KB  
Article
From Susceptibility to Severity: The Impact of Interleukin-33 rs1929992 Polymorphism on Asthma in a Taiwanese Population
by Te-Chun Hsia, Liang-Wen Hang, Te-Chun Shen, Jie-Long He, Kai-Ling Huang, Ding-Han Chen, Yun-Chi Wang and Da-Tian Bau
Life 2026, 16(9), 1395; https://doi.org/10.3390/life16091395 - 24 Aug 2026
Abstract
Asthma is a chronic inflammatory airway disease strongly influenced by genetic factors. Interleukin-33 (IL-33), a key mediator of type 2 immune responses, has been implicated in airway inflammation and remodeling. However, the effects of IL-33 polymorphisms on asthma susceptibility and severity [...] Read more.
Asthma is a chronic inflammatory airway disease strongly influenced by genetic factors. Interleukin-33 (IL-33), a key mediator of type 2 immune responses, has been implicated in airway inflammation and remodeling. However, the effects of IL-33 polymorphisms on asthma susceptibility and severity remain unclear, particularly in East Asian populations. This study investigated five IL-33 polymorphisms (rs1891385, rs16924159, rs12551256, rs1929992, and rs7044343) in relation to asthma risk and severity in Taiwanese individuals. A total of 198 asthmatic patients and 453 age- and sex-matched controls were enrolled. Genotypes were determined using PCR-RFLP. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to assess associations with asthma susceptibility and severity. Among the five polymorphisms, only rs1929992 was significantly associated with asthma. Compared with the TT genotype, CT and CC carriers had reduced asthma risk (OR = 0.61 and 0.51, respectively). The dominant model (CT+CC) also showed a protective effect (OR = 0.58, 95%CI = 0.40–0.82, p = 0.0032), which was supported by allelic analysis (OR = 0.70, 95%CI = 0.55–0.89, p = 0.0044). Among the five polymorphisms, rs1929992 was associated with asthma susceptibility. Under the dominant model, CT + CC carriers showed lower odds of asthma than TT carriers (OR = 0.58, 95% CI = 0.40–0.82, p = 0.0032), and the association remained significant after correction for multiple testing. Exploratory stratified analyses identified associations in the younger and male subgroups, while exploratory severity analysis suggested lower odds of more severe asthma among variant genotype carriers. These secondary findings should be considered hypothesis-generating because of the reduced subgroup sample sizes. Overall, rs1929992 was associated with asthma susceptibility in this Taiwanese population; however, independent replication and functional studies are required before its biological or clinical relevance can be established. Full article
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