Fatih Ciftci, Kadriye Yasemin Usta Ayanoğlu, Azime Erarslan
{"title":"Bridging Clinical Microbiology and Artificial Intelligence: An Image-Based Deep Learning Framework for Automated Antimicrobial Susceptibility Testing.","authors":"Fatih Ciftci, Kadriye Yasemin Usta Ayanoğlu, Azime Erarslan","doi":"10.1016/j.bj.2026.100965","DOIUrl":"https://doi.org/10.1016/j.bj.2026.100965","url":null,"abstract":"<p><p>The rising threat of antimicrobial resistance has underscored the urgent need for rapid, standardized, and automated antimicrobial susceptibility testing (AST) solutions. Leveraging recent advances in computer vision and deep learning, this study introduces a fully image-based diagnostic framework that integrates a YOLOv8n object detection model with a Convolutional Neural Network (CNN) to perform end-to-end bacterial identification and susceptibility classification directly from Petri dish images. The YOLOv8n model accurately localizes handwritten bacterial species labels with a mean Average Precision (mAP@0.50) exceeding 0.93, demonstrating robustness across diverse handwriting styles and imaging conditions. Complementarily, the CNN achieves a balanced accuracy of 94.7% and 100% sensitivity for susceptible cases by analyzing inhibition zone morphology without manual measurements or interpretive rules. Notably, the system achieved a 0% Very Major Error (VME) rate, ensuring no resistant isolates were misclassified as susceptible. The dual-model system generalizes effectively across experimental variations and produces high-confidence predictions, highlighting its potential to streamline AST workflows, minimize human variability, and enhance diagnostic reliability in clinical microbiology.</p>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":" ","pages":"100965"},"PeriodicalIF":4.4,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147455582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The complex interplay between hepatitis D virus and the interferon response.","authors":"Claudie Eber, Eloi R Verrier","doi":"10.1016/j.bj.2026.100964","DOIUrl":"https://doi.org/10.1016/j.bj.2026.100964","url":null,"abstract":"<p><p>Hepatitis D virus (HDV) infection represents a major global public health challenge and is responsible for the most severe form of chronic viral hepatitis. Affecting an estimated 12 million individuals worldwide, chronic hepatitis D is associated with rapid progression to advanced liver disease, including cirrhosis and hepatocellular carcinoma. Despite its clinical burden, therapeutic options for HDV remain limited. In this context, pegylated interferon alpha (PEG-IFN-α) continues to be the most widely used treatment globally, particularly outside Europe where access to newly approved therapies is restricted. However, PEG-IFN-α is characterized by modest and heterogeneous antiviral efficacy, frequent viral relapse, and a high rate of adverse effects, highlighting the need for improved therapeutic strategies. A better understanding of the mechanisms underlying interferon responsiveness and resistance in HDV infection is therefore essential. The complex interplay between HDV and the innate immune response plays a central role in determining viral persistence and treatment outcome. HDV is sensed by innate immune receptors and induces type I and type III interferon responses, yet these responses are insufficient to control viral replication. Viral nuclear replication, interferon-stimulated gene accessibility, and active interference with interferon signaling pathways contribute to the limited antiviral activity of interferons against HDV. This review synthesizes current knowledge on the interactions between HDV and the interferon response, discusses experimental models used to study these mechanisms, and highlights key limitations and open questions that must be addressed to optimize future interferon-based and combination therapies.</p>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":" ","pages":"100964"},"PeriodicalIF":4.4,"publicationDate":"2026-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147389270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Comparison of Tear Function in Patients With and Without Mental Disorders: A Systematic Review and Meta-analysis.","authors":"Yen-Jung Chen, Chia-Chao Liu, Chi-Chin Sun, Chi-Chun Lai, Ching-Yen Chen, Shih-Chieh Shao","doi":"10.1016/j.bj.2026.100963","DOIUrl":"https://doi.org/10.1016/j.bj.2026.100963","url":null,"abstract":"<p><strong>Background: </strong>Eye care is crucial for patients with mental disorders, yet it is often overlooked. Previous studies suggest a link between mental disorders and dry eye disease, but results on objective tear function are inconsistent. This meta-analysis aimed to compare tear function between patients with and without mental disorders.</p><p><strong>Methods: </strong>We systematically searched Embase, PubMed, Cochrane and PsycINFO up to November 19, 2025. We included studies reporting the comparison of tear function outcomes measured by the Schirmer test or tear break-up time (TBUT) between adult patients with and without mental disorders. The meta-analysis based on a random-effects model presented pooled mean differences between groups.</p><p><strong>Results: </strong>We included 15 studies with a total of 3,319 participants. Our meta-analysis revealed that patients with mental disorders had lower TBUT (MD: -3.72, 95% CI: -5.76 to -1.69, I<sup>2</sup>: 99%) and Schirmer test (MD: -4.62, 95% CI: -7.42 to -1.83, I<sup>2</sup>: 98%). Results remained consistent across subgroup analyses based on gender, study country, psychiatric diagnosis, psychiatric medication use and study design. Notably, significantly lower Schirmer test results were observed even in patients not receiving psychiatric medication.</p><p><strong>Conclusion: </strong>Compared to patients without mental disorders, patients with mental disorders were associated with poor tear function. Regular monitoring and early detection of tear dysfunction should be considered for patients with mental disorders. However, due to the substantial heterogeneity and the cross-sectional design of most included studies, the findings should be interpreted with caution and are best viewed as hypothesis-generating.</p>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":" ","pages":"100963"},"PeriodicalIF":4.4,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147316433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Revisiting the Safety of Short-term Systemic Corticosteroids: Safety of short-term systemic corticosteroids.","authors":"Hui-Ju Tsai, Tsung-Chieh Yao","doi":"10.1016/j.bj.2026.100962","DOIUrl":"https://doi.org/10.1016/j.bj.2026.100962","url":null,"abstract":"<p><p>Short-term systemic corticosteroids are widely prescribed to treat acute flare-ups of chronic immunologic diseases or to manage acute inflammatory conditions such as allergic reactions, skin disorders, and respiratory infections. This review revisits the safety of short-term systemic corticosteroids, focusing on emerging evidence of their potential unexpected risks. Epidemiological studies reveal an increasing trend in the prescribing of short-term systemic corticosteroids to the general population. However, concerns have been raised regarding the safety of short-term oral corticosteroids, with recent evidence suggesting that even brief courses are associated with rare but serious adverse events, including sepsis, pneumonia, gastrointestinal bleeding, acute pancreatitis, heart failure, venous thromboembolism, and fracture. Recent studies also highlight long-term risks of antenatal corticosteroids. While crucial for reducing neonatal respiratory distress syndrome in pregnancies at risk of preterm delivery, antenatal corticosteroids are linked to long-term risks of neuropsychiatric disorders, serious infections, and even mortality in children, along with heightened risks of infections, heart failure, and gastrointestinal bleeding in mothers. These findings suggest the potential harms of short-term systemic corticosteroids may have been previously underrecognized. Raising awareness of these risks can help clinicians balance therapeutic benefits with potential harms and ensure safer clinical practice. Cautious and evidence-based approaches to prescribing short-term systemic corticosteroids are necessary, particularly in vulnerable populations. Further research is needed to develop a \"corticosteroid stewardship\" approach that promotes prescribing systemic corticosteroids only for appropriate indications, minimizes unnecessary use, and encourages careful monitoring of adverse effects to optimize patient outcomes.</p>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":" ","pages":"100962"},"PeriodicalIF":4.4,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146218392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yu-Qian Jiang, Qing-Yu Kuang, Yuan Xu, Yi-Xiang Xu, Jie Cheng, Li-Tao Yi
{"title":"GR/HDAC2/synaptic complexes in hippocampal CA1 mediate the antidepressant effects of magnolol.","authors":"Yu-Qian Jiang, Qing-Yu Kuang, Yuan Xu, Yi-Xiang Xu, Jie Cheng, Li-Tao Yi","doi":"10.1016/j.bj.2026.100961","DOIUrl":"https://doi.org/10.1016/j.bj.2026.100961","url":null,"abstract":"<p><strong>Background: </strong>Depression is a multifactorial neuropsychiatric disorder linked to neuroinflammation and epigenetic dysregulation, particularly in histone acetylation. Although magnolol has demonstrated antidepressant-like properties, its precise molecular mechanisms remain unclear. This study aimed to evaluate the antidepressant effects of magnolol and its influence on epigenetic regulation of synaptic plasticity in a chronic unpredictable mild stress (CUMS) mouse model.</p><p><strong>Material and methods: </strong>C57BL/6 mice subjected to CUMS were treated orally with magnolol. Depressive-like behaviors were assessed using standard behavioral tests. Expression levels of histone deacetylase 2 (HDAC2), synaptic proteins such as neuroligin-1 (NLGN1) and neurexin-1β (NRXN1β), and their associated co-localized puncta were examined. Golgi staining and immunofluorescence were performed to assess dendritic spine density and DCX-positive cell population in the hippocampus.</p><p><strong>Results: </strong>Magnolol treatment alleviated depressive-like behaviors, evidenced by increased sucrose preference and reduced immobility in behavioral assays. It also attenuated hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, as shown by normalization of serum corticosterone levels and restoration of glucocorticoid receptor (GR) expression in the hippocampal CA1 region. At the molecular level, magnolol reduces HDAC2 expression, which may be associated with altered histone acetylation, thus upregulation of NLGN1 and NRXN1β, enhancing the formation of pre- and postsynaptic co-localized puncta. Additionally, magnolol promoted hippocampal DCX-positive cell population and synaptogenesis, supporting improvements in structural and functional neuroplasticity.</p><p><strong>Conclusion: </strong>Our findings demonstrate the ability of magnolol to modulate histone acetylation and synaptic architecture involved in its antidepressant-like action. These results provide a foundation for further exploration of magnolol-based interventions targeting epigenetic and synaptic mechanisms in depression.</p>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":" ","pages":"100961"},"PeriodicalIF":4.4,"publicationDate":"2026-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146194088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Age-Dependent Effects of Losartan and Exercise on Skeletal Muscle Redox Balance and Protein Turnover in Mice.","authors":"Chung-Hao Lin, Po-Cheng Chang, Jyh-Jeen Yang, Gwo-Jyh Chang, Chiao-Nan Chen","doi":"10.1016/j.bj.2026.100951","DOIUrl":"https://doi.org/10.1016/j.bj.2026.100951","url":null,"abstract":"<p><strong>Background: </strong>Aging is associated with impaired muscle protein turnover, oxidative stress, and functional decline. Both renin-angiotensin system (RAS) inhibition and exercise modulate redox balance and anabolic-catabolic signaling; however, how aging influences their effects under physiological conditions remains unclear.</p><p><strong>Methods: </strong>Middle-aged (50 weeks) and old (72 weeks) female C57BL/6 mice were randomly assigned to control (C), losartan (L; RAS inhibitor), exercise (E), or combined losartan plus exercise (LE) groups for a four-month intervention. Exercise capacity, cardiac function, oxidative stress markers [thiobarbituric acid reactive substances (TBARS) and total antioxidant capacity (TAC)] in skeletal muscles, and key regulators of muscle protein turnover (Akt, mTOR, ERK1/2, Smad2, FoxO3a, and p38 MAPK) were evaluated. Two-way analysis of variance was used to determine whether age influences the effects of interventions.</p><p><strong>Results: </strong>Exercise training (E and LE) improved exercise capacity in both age groups. The combined LE intervention significantly enhanced cardiac systolic function compared to exercise alone. Losartan exerted age-dependent, opposite redox effects. In middle-aged mice, losartan increased TBARS and reduced TAC. Conversely, in old mice, losartan significantly reduced TBARS and increased TAC. Most protein turnover regulators (Akt, mTOR, ERK, FoxO3a, and p38 MAPK) remained unchanged by interventions, while Smad2 activation exhibited age-dependent patterns. Smad2 activation levels increased in middle-aged LE mice but were reduced by exercise in old mice.</p><p><strong>Conclusions: </strong>While exercise is a robust intervention, losartan's efficacy is critically dependent on the animal's baseline oxidative status. These findings highlight the importance of considering age as a critical factor when designing pharmacological interventions for age-related muscle atrophy.</p>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":" ","pages":"100951"},"PeriodicalIF":4.4,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146117679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Biomedical JournalPub Date : 2026-02-01Epub Date: 2026-01-29DOI: 10.1016/j.bj.2026.100950
Aila Akosua Kattner
{"title":"From inhibition to regulation: serpins in health and disease","authors":"Aila Akosua Kattner","doi":"10.1016/j.bj.2026.100950","DOIUrl":"10.1016/j.bj.2026.100950","url":null,"abstract":"<div><div>This issue of the Biomedical Journal highlights regulatory mechanisms that shape aging, disease progression, and biological complexity across molecular, cellular, and systems levels. A central theme is plasminogen activator inhibitor-1 (PAI-1) as a multifunctional regulator linking fibrinolysis, cellular senescence, stem cell dynamics, fibrosis, and tumor biology. Contributions examine structure-guided development of small-molecule PAI-1 inhibitors and their therapeutic potential across thrombotic disease, chronic myeloid leukemia, systemic sclerosis, lung cancer, and skin cancer, emphasizing controlled modulation of PAI-1 activity to preserve physiological balance while overcoming disease-associated dysregulation. Beyond protease signaling, several studies address regulatory layers governing cellular state and adaptability. Epitranscriptomic remodeling via N6-methyladenosine (m6A) emerges as a key mechanism in protozoan parasites and host–pathogen interactions, including parasite-driven reprogramming of host leukocytes. In cancer biology, ferroptosis susceptibility is shown to be regulated through SLC7A11-associated protein interactions, linking redox homeostasis, cell survival, and tumor progression in hepatocellular carcinoma. Exosome-mediated intercellular communication is further examined as a mechanism regulating tissue repair, inflammation, and systemic crosstalk, including gut microbiota–dependent effects on bone homeostasis. Methodological advances further underscore the importance of precision and interpretability in modern biomedical research. These include accessible platforms for reproducible single-cell RNA sequencing analysis, robot-assisted quantification of acupuncture mechanics underlying analgesic responses, and interpretable deep-learning frameworks combining classification and segmentation in medical imaging. Quantitative three-dimensional imaging approaches are also applied to craniofacial surgery, where cone-beam computed tomography–based analyses identify determinants of lip cant and facial midline correction following bimaxillary surgery. A conceptual synthesis places living systems and learning systems within shared theoretical frameworks, highlighting the convergence of physics, information theory, and artificial intelligence in understanding biological organization.</div></div>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":"49 1","pages":"Article 100950"},"PeriodicalIF":4.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146075987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Biomedical JournalPub Date : 2026-02-01Epub Date: 2025-09-05DOI: 10.1016/j.bj.2025.100911
Takeshi Masuda , Noboru Hattori
{"title":"Role of PAI-1 in the progression and treatment resistance of non-small cell lung cancer","authors":"Takeshi Masuda , Noboru Hattori","doi":"10.1016/j.bj.2025.100911","DOIUrl":"10.1016/j.bj.2025.100911","url":null,"abstract":"<div><h3>Background</h3><div>Lung cancer is the leading cause of cancer-related mortality worldwide. Although immune checkpoint inhibitors (ICIs), chemotherapy, and molecular targeted therapies have improved survival rates, therapeutic resistance remains a major barrier to curative outcomes. Recently, plasminogen activator inhibitor-1 (PAI-1) has been implicated in lung cancer progression and treatment resistance.</div></div><div><h3>Material and methods</h3><div>This review summarizes the recent evidence from preclinical and clinical studies on the role of PAI-1 in the progression and treatment resistance in lung cancer, focusing on its contribution to tumor aggressiveness and resistance to therapy. As limited evidence is available regarding its role in small cell lung cancer, this review focuses on the findings reported to date for non-small cell lung cancer (NSCLC).</div></div><div><h3>Results</h3><div>PAI-1 promoted tumor invasion, angiogenesis, and epithelial–mesenchymal transition (EMT), thereby facilitating cancer progression. Elevated PAI-1 expression in tumor tissues and plasma is correlated with advanced disease stages and poor prognosis. Genetic polymorphisms such as A15T, which affect PAI-1 stability, are also associated with unfavorable outcomes. PAI-1 contributes to radiotherapy resistance through the hypoxia-induced upregulation of AKT/ERK signaling, chemotherapy by activating cancer-associated fibroblasts, and targeted therapies via integrin-mediated EMT. Moreover, it enhances immune evasion by promoting programmed cell death-ligand 1 expression and creating an immunosuppressive tumor microenvironment.</div></div><div><h3>Conclusions</h3><div>PAI-1 is a key regulator of tumor progression and therapeutic resistance in NSCLC. Targeting PAI-1 may offer a novel strategy to overcome resistance to multiple treatment modalities, and future research should focus on developing PAI-1–based biomarkers and therapeutic combinations for both NSCLC.</div></div>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":"49 1","pages":"Article 100911"},"PeriodicalIF":4.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145013804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Biomedical JournalPub Date : 2026-02-01Epub Date: 2025-12-13DOI: 10.1016/j.bj.2025.100933
Emily Wittrup , Alan Kay , Jett Rosen , Kuan-Fu Chen , Kayvan Najarian
{"title":"The legacy and future of recurrent neural networks in personalized medicine: A reflection on the 2024 Nobel Physics Prize","authors":"Emily Wittrup , Alan Kay , Jett Rosen , Kuan-Fu Chen , Kayvan Najarian","doi":"10.1016/j.bj.2025.100933","DOIUrl":"10.1016/j.bj.2025.100933","url":null,"abstract":"<div><div>The 2024 Nobel Physics Prize was awarded to Geoffrey Hinton and John Hopfield for their pioneering contributions to neural networks and artificial intelligence (AI), marking a significant milestone in AI’s development, particularly in the potential integrations into personalized medicine. This article surveys the profound influence of Hopfield’s and Hinton’s foundational work, tracing the development of recurrent neural networks (RNNs) from early associative memory models to advanced deep learning architectures. We delve into how contemporary RNN architectures are transforming personalized medicine by improving diagnostic accuracy, facilitating image analysis, generating radiology reports, and estimating individual treatment effects. Despite advancements, current challenges such as model interpretability, generalizability, and ethical considerations in AI application demand further exploration. This article posits that future RNN development will blend rigorous algorithmic insights with powerful generative capabilities to advance both medical applications and theoretical understanding. We conclude with a reflection on the future trajectory of RNNs in AI, underscoring a need for balancing computational efficiency with transparency and adaptability in healthcare environments.</div></div>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":"49 1","pages":"Article 100933"},"PeriodicalIF":4.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145762121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Dynamic regulation of RNA m6A methylation in the ribonucleoprotein complexes in apicomplexan and kinetoplastid parasites","authors":"Kaitlin Klotz, Carli Camporeale, Kausik Chakrabarti","doi":"10.1016/j.bj.2025.100903","DOIUrl":"10.1016/j.bj.2025.100903","url":null,"abstract":"<div><div>m<sup>6</sup>A, or N<sup>6</sup>-methyladenosine, is the most abundant modification of mRNA transcripts. These modifications are known to influence mRNA transcript stability, transcription, translation, alternative splicing and decay, with undoubtedly more functions to be discovered. In this review, we explored the roles of m<sup>6</sup>A modifications in two groups of protozoan parasites: the apicomplexans, which include <em>Plasmodium</em> and <em>Toxoplasma</em> species, and kinetoplastids, which include <em>Trypanosoma</em> and <em>Leishmania</em> species. We also compared the key players of m<sup>6</sup>A epitranscriptomic machinery in creating, interpreting, and removing m<sup>6</sup>A modifications between these parasitic protists as well as a discussion of how m<sup>6</sup>A modifications facilitate parasite survival through features specific to apicomplexans and kinetoplastids. Beyond parasite epitranscriptomes, this review compares m<sup>6</sup>A dynamics in host and vector species (humans, flies and mosquitoes), highlighting coevolutionary adaptations. Strikingly, both the parasites and their vectors lack canonical m<sup>6</sup>A demethylases, implying a largely irreversible, streamlined m<sup>6</sup>A landscape fine-tuned for synchronized gene regulation. Overall, a mechanistic understanding is emerging of how m<sup>6</sup>A-modified RNAs and their binding proteins orchestrate RNA processing, translation, and turnover in parasitic protists, revealing an evolutionarily tuned epitranscriptomic system.</div></div>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":"49 1","pages":"Article 100903"},"PeriodicalIF":4.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144941112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}