Current molecular medicine最新文献

{"title":"Development of Integrated Turbidity Spectrophotometric Biosensor System with Osmotic Fragility/DichlorophenolIndophenol Precipitation Assays for Thalassemia Red Blood Cell Screening.","authors":"Preeya Pramool, Surakiate Wanram, Kanathip Butchai, Purinut Charoenrat, Somkid Pencharee, Surasak Wanram","doi":"10.2174/0115665240429789260211021243","DOIUrl":"https://doi.org/10.2174/0115665240429789260211021243","url":null,"abstract":"<p><strong>Introduction: </strong>Thalassemia remains a major public health burden, particularly in low-resource regions where access to advanced laboratory diagnostics is limited. Although high-performance liquid chromatography (HPLC) and capillary electrophoresis (CE) provide reliable hemoglobin characterization, their cost, infrastructure requirements, and turnaround time restrict large-scale screening. From a practical screening perspective, there is a clear need for a rapid, portable, and objective point-of-care (POC) approach that supports early identification and appropriate referral.</p><p><strong>Methods: </strong>We developed an integrated turbidity spectrophotometric biosensor that quantitatively combines the osmotic fragility (OF) test and the dichlorophenolindophenol precipitation (DCIP) clear assay. The system employs a portable LEDbased spectrophotometric reader controlled by an ESP32 microcontroller, integrated with real-time web-based visualization and automated interpretation. Ninety-nine EDTA blood specimens were analyzed. Red blood cell fragility and hemoglobin stability were assessed using time-resolved absorbance slope measurements at 540 and 600 nm for OF and DCIP, respectively. Analytical reproducibility, diagnostic performance, and agreement with reference methods were evaluated.</p><p><strong>Results: </strong>The biosensor demonstrated high analytical reproducibility, with mean coefficients of variation of 2.8% for OF slopes and 3.5% for DCIP slopes. Diagnostic performance was robust, yielding AUC values of 0.94 for OF and 0.90 for DCIP. An integrated decision algorithm achieved an overall concordance of 90.2% with goldstandard methods and provided preliminary interpretation within 3 minutes through a secure web-based dashboard.</p><p><strong>Discussion: </strong>Quantitative integration of OF and DCIP assays within a single platform improves screening objectivity while maintaining rapid turnaround, supporting decentralized and point-of-care testing.</p><p><strong>Conclusion: </strong>This integrated turbidity biosensor offers a rapid and scalable POC solution for preliminary thalassemia screening in underserved settings. Future development will focus on mobile integration, secure linkage with public health systems, and incorporation of additional hematologic or molecular parameters to further enhance diagnostic confidence.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbiota-driven Immunopathogenesis in Systemic Lupus Erythematosus: Cross-site Mechanisms and Intervention Strategies.","authors":"Shuqing Feng, Qin Huang","doi":"10.2174/0115665240433654260209063544","DOIUrl":"https://doi.org/10.2174/0115665240433654260209063544","url":null,"abstract":"<p><p>Systemic lupus erythematosus (SLE) is a complex autoimmune disease whose pathogenesis involves intricate interactions with the human microbiota. Accumulating evidence reveals significant compositional and functional dysbiosis in the gut, oral, skin, and vaginal microbiota of SLE patients compared to healthy individuals. These dysbioses actively contribute to disease development and progression through a multitude of mechanisms. These include impaired epithelial barrier integrity, exemplified by the \"leaky gut\" phenomenon, which facilitates the translocation of microbial antigens. Molecular mimicry, where microbial antigens share structural similarities with host self-antigens, triggers the production of cross-reactive autoantibodies. Furthermore, dysregulated production of microbial metabolites, such as short-chain fatty acids, tryptophan derivatives like tryptamine, and histamine, directly modulates host immune cell function, promotes inflammatory responses, and influences epigenetic regulation. The causal role of specific microbiota in SLE is substantiated by experimental models, including fecal microbiota transplantation studies where transfer of SLE-associated microbiota can recapitulate autoimmune features in recipient germ-free mice, and mono-colonization with pathobionts like Ruminococcus gnavus or Staphylococcus aureus can drive specific aspects of the disease. This growing understanding has paved the way for novel microbiota-targeting interventions. Strategies such as dietary modifications, probiotic and prebiotic supplementation, and fecal microbiota transplantation show considerable promise in preclinical and early clinical studies for restoring microbial homeostasis, rebalancing dysregulated immune responses, and alleviating disease activity. However, challenges in patient-specific variability, understanding precise mechanisms, and ensuring longterm safety remain. Future research must focus on delineating detailed causal pathways, validating efficacy in large-scale trials, and ultimately developing personalized microbiota-targeting interventions to improve SLE management and patient outcomes.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Systematic Review and Meta-Analysis of Immune Signatures Involved in the Prevalence of Exhaustion in Humans, Mice, and Bovine Species.","authors":"Khushbu Sharma, Shalini Sharma, Shweta Dhanda, Saurabh Gupta, Shivalingappa Yamanappa Mukartal, Sarvesh Rustagi, Kundan Kumar Chaubey, Sanjay Kumar","doi":"10.2174/0115665240414612260116235015","DOIUrl":"https://doi.org/10.2174/0115665240414612260116235015","url":null,"abstract":"<p><strong>Introduction: </strong>Immune exhaustion is known to occur in chronic infections as well as cancer, and is characterized by constant antigenic stimulation and gradual loss of T cell function and upregulation of immune exhaustion markers. This systematic review aims to explore conserved and divergent exhaustion signatures across humans, mice, and bovines to advance our understanding for better translational outcomes.</p><p><strong>Methods: </strong>Following PRISMA 2020 guidelines, studies from 2011-2023 were analyzed using a random-effects model (metaprop, logit transformation). Subgroup analyses (species, disease type), sensitivity and heterogeneity (I²) analyses were performed. Publication bias was performed to evaluate biomarker variability.</p><p><strong>Results: </strong>Meta-analysis identified an almost consistent role of IL-6 (48%), IL-2 (51%), TNF-α (46%), IFN-γ (41%), and IL-10 (48%) in immune exhaustion throughout various chronic disease conditions. Co-inhibitory receptors such as PD-1 (51%), TIM-3 (54%), LAG-3 (59%), and CTLA-4 (64%) were highly upregulated. Extreme heterogeneity (I² >95%) pointed towards considerable variation mainly due to species differences, disease category, and methodological factors, with fewer murine and bovine studies compared to human literature.</p><p><strong>Discussion: </strong>The confluence of pro-inflammatory cytokines with elevated checkpoint receptor expression highlights the fact that immune exhaustion is conserved across mammals. However, the limitation in extrapolation attributed to high heterogeneity and species imbalance exists in the study. Furthermore, the variations in disease models and technical differences in detection methods point towards a need for standardization and integrated comparative analyses to boost biomarker interpretation.</p><p><strong>Conclusion: </strong>Co-inhibitory receptors and various cytokines appear to be the conserved contributors to immune exhaustion across species. Further, enriching cross-species data sets and accounting for methodological variability will improve the translational importance and support in developing more precise therapeutic interventions.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147621695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Synergistic Effect of Nutlin-3a and a Wip1 Inhibitor in Inducing p53 Activity.","authors":"Ali Hikmat Alburghaif, Hany Akeel Al-Hussaniy, Ali Mahmoud Al-Samydai, Zainab Malik Saleem, Alhasan Ali Jabbar","doi":"10.2174/0115665240437546260121175241","DOIUrl":"https://doi.org/10.2174/0115665240437546260121175241","url":null,"abstract":"<p><strong>Introduction: </strong>The p53 protein plays a major role in maintaining genome stability as well as the response of cells to stress. One of the principal things that regulates p53 is MDM2, and the way it interacts with p53 is of great significance in the degradation of p53. This dephosphorylation of p53 by Wip1 increases its affinity to MDM2, which causes p53 degradation. Wip1 is used to increase the growth of tumors by undermining the p53 pathway. However, the active form of p53 can be retained with the help of preventing Wip1, and this fact makes it useful as a target of cancer treatment. An ever-increasing body of preclinical evidence suggests the possibility that Wip1 inhibitors would be used alongside potent MDM2 inhibitors to enhance p53 activity and enhance treatment outcomes. The purpose of the review was to examine studies pertaining to the action of a Wip1 inhibitor and Nutlin-3a in order to induce p53 functionality.</p><p><strong>Method: </strong>We searched Google Scholar, PubMed, and other search engines using such terms as MDM2 inhibitors, Wip1 inhibitors, and Nutlin. Newer articles published after 2020 were chosen to ensure that the recent findings are included.</p><p><strong>Results: </strong>Wip1, an attractive antineoplastic target to control the p53 pathway, is a dephosphorylator of p53 at serine-15. Nutlin-3a with a Wip1 inhibitor appears to act synergistically to push p53 half-maximal inhibitory concentrations (IC50) into the low micromolar range. This combination greatly stimulates downstream p53-dependent response, which leads to a strong reduction of cell proliferation.</p><p><strong>Discussion: </strong>We find that MDM2 inhibitors in combination with Wip1 inhibitors are synergistic in stimulating p53 activity. The results emphasize the need to use a combination of p53 induction and the inactivation of its suppressors in the treatment of cancer.</p><p><strong>Conclusion: </strong>As p53 is the most commonly mutated gene across a broad range of tumors, enhancing p53 activity is a prerequisite for achieving potent therapeutic effects. We envision that combination therapies involving Nutlin-3a, Wip1 inhibitors, and other effective cancer treatments may synergistically improve p53 activity and enhance therapeutic outcomes.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147621705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic Changes of Extracellular Matrix in Sepsis: A Review.","authors":"Mingjie Fu, Wenwei Xu, Jie Zhao, Shi Fu, Shuiqiao Fu, Liang Ma","doi":"10.2174/0115665240407854251202120058","DOIUrl":"https://doi.org/10.2174/0115665240407854251202120058","url":null,"abstract":"<p><p>During the pathogenesis of sepsis, extracellular matrix (ECM) impairment represents a critical pathological hallmark. The ECM not only plays pivotal roles in maintaining tissue architecture and physiological functions, but also actively participates in cellular signaling transduction and tissue repair mechanisms. Sepsisinduced systemic inflammatory responses and oxidative stress provoke ECM component degradation and structural remodeling, which, in turn, activate multiple intracellular and intercellular signaling cascades. Bioactive fragments derived from ECM degradation can function as signaling ligands that bind to specific cell surface receptors, triggering downstream pathways that regulate critical cellular processes, including survival, proliferation, migration, and inflammatory activation. The sustained activation of these signaling networks exerts profound pathophysiological consequences, potentially leading to vascular endothelial dysfunction, dysregulated immune cell hyperactivation, and coagulation system abnormalities. Furthermore, these signaling pathways mediate essential regulatory functions during the tissue remodeling phase in late-stage sepsis. While this dynamic ECM remodeling may facilitate tissue repair and regeneration, persistent dysregulation could result in maladaptive fibrosis and permanent organ dysfunction. Collectively, the ECM demonstrates multifaceted involvement in sepsis pathophysiology through its regulatory effects on cellular signaling, functional modulation, and tissue remodeling processes. This article systematically synthesizes current knowledge regarding ECM dynamics in sepsis pathogenesis.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147303480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional Roles of Non-Coding RNAs in Graves' Disease.","authors":"Omid Anbiyaee, Abdolah Mousavi Salehi, Bahar Jaberian Asl, Fatemeh Jamshidi, Farhoodeh Ghaedrahmati, Maryam Farzaneh","doi":"10.2174/0115665240380518251113092158","DOIUrl":"https://doi.org/10.2174/0115665240380518251113092158","url":null,"abstract":"<p><p>Graves' disease (GD) is a disorder marked by an enlarged and overactive thyroid gland (Graves' hyperthyroidism), ocular abnormalities (Graves' orbitopathy; GO), and localized dermopathy (pretibial myxoedema; PTM). It is recognized as the most common cause of hyperthyroidism worldwide. Patients with GD most frequently exhibit elevated thyroid hormone secretion from thyroid cells as a result of autoantibodies acting as thyroid-stimulating hormone receptor (TSHR) agonists. Numerous investigations have examined the elements that contribute to the pathogenesis of GD, focusing on different components, such as molecular factors like non-coding RNAs (ncRNAs). NcRNAs represent a type of RNA transcript that, while not encoding proteins, are essential in the regulation of numerous aspects of cellular biology. NcRNAs include major groups, such as circular RNAs (circRNAs), long noncoding RNAs (lncRNAs), and small non-coding RNAs (sncRNAs), all of which are garnering increasing interest in the scientific community. This review will provide a comprehensive analysis of the function of ncRNAs in the development, diagnosis, and treatment of GD, and investigate the latest research in this area.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146225727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alterations in the Expression of Toll-Like Receptors (TLRs) 3, 4, and 7 in Patients with COVID-19: The Role of Disease Severity and Gender.","authors":"Zohreh-Al-Sadat Ghoreshi, Mohsen Sharif-Zak, Gholamreza Asadikaram, Mojtaba Abbasi-Jorjandi, Alireza Afsharipur, Fatemeh Seyedi, Hamidreza Reshidinejad, Mohammad Kazemiarababadi, Fardin Khajepour, Nasir Arefinia, Moslem Abolhassani","doi":"10.2174/0115665240394369251208174759","DOIUrl":"https://doi.org/10.2174/0115665240394369251208174759","url":null,"abstract":"<p><p><P> Introduction: The expression dynamics of Toll-like receptors (TLRs) in response to SARS-CoV-2, particularly regarding disease severity, remain poorly understood. This study aimed to investigate the gene expression of TLR3, TLR4, and TLR7 in COVID-19 patients and correlate them with disease severity and gender. </P> <P> Methods: This case-control study enrolled 470 COVID-19 patients (categorized as moderate, severe, and critical) and 100 healthy controls. The mRNA expression levels of these genes in peripheral blood leukocytes were quantified using RT-qPCR. </P> <P> Results: Expression of all three TLRs was significantly higher in patients than in the control group. Overall, male patients exhibited higher expression than females. Notably, a significant decrease in TLR3, TLR4, and TLR7 expression was observed in the critical group compared with the moderate and severe groups. </P> <P> Discussion: This paradoxical downregulation of TLRs in critical patients, reported for the first time in such a large cohort (N=470), aligns with reports of 'immunoparalysis' or 'immune exhaustion' observed in other severe inflammatory conditions. This phenomenon might represent a negative feedback mechanism to prevent overwhelming systemic inflammation, although it may concurrently compromise pathogen clearance. </P> <P> Conclusion: The findings suggest that while TLR expression is upregulated in COVID-19, its downregulation in critical stages may be associated with an unfavorable disease outcome. Therefore, TLR expression levels could be considered potential biomarkers for identifying patients at risk of progressing to the critical phase of the disease.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA HULC/miR-556-5p Axis Attenuates Ang II-Induced Cardiac Microvascular Endothelial Cell Dysfunction by Suppressing the AMPK/FOXO3 Pathway.","authors":"Yafeng Hao, Mingming Fu, Zhiqian Wang","doi":"10.2174/0115665240395360251112160900","DOIUrl":"https://doi.org/10.2174/0115665240395360251112160900","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to investigate the regulatory mechanism of the LncRNA HULC/miR-556-5p axis in endothelial cell injury associated with heart failure and its impact on endothelial cell function. Specifically, we explored how HULC interacts with miR-556-5p to modulate cell survival, apoptosis, inflammation, and autophagy in response to Ang II-induced injury.</p><p><strong>Methods: </strong>Human cardiac microvascular endothelial cells (HCMECs) were utilized as the study model. Ang II-induced HCMEC injury was simulated by treating cells with 100 nM Ang II for 24 hours. The expression levels of HULC, miR-556-5p, and related proteins were assessed using techniques, such as real-time quantitative PCR and Western blot. Cell apoptosis was detected using flow cytometry, and inflammatory cytokine release (TNF-α, IL-1β, and IL-6) was analyzed via ELISA. Cell viability was assessed using MTT assays. Immunoblotting was employed to evaluate the phosphorylation status of key signaling molecules, including AMPK and FOXO3.</p><p><strong>Results: </strong>We observed a crucial role of the LncRNA HULC/miR-556-5p axis in Ang IIinduced HCMEC injury. Overexpression of HULC significantly suppressed miR-556-5p activity, thereby reducing cell apoptosis and the release of inflammatory cytokines while promoting cell survival. Further experimental results indicated that miR-556-5p regulated cell function by reducing the expression level of FOXO3 and modulating the AMPK signaling pathway. Additionally, miR-556-5p markedly decreased cellular autophagy levels, further supporting its regulatory role in endothelial cell injury associated with heart failure.</p><p><strong>Conclusion: </strong>This study elucidates the important role of the LncRNA HULC/miR-556- 5p axis in endothelial cell injury associated with heart failure. Our findings provide new insights into the pathophysiological mechanisms of heart failure and highlight the potential therapeutic value of targeting this axis to improve endothelial cell function.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146060766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphatidylethanolamine: Structural Component and Beyond.","authors":"Swaroop Kumar Pandey, Ayush Kulshreshtha, Anuja Mishra","doi":"10.2174/0115665240415642251205104453","DOIUrl":"https://doi.org/10.2174/0115665240415642251205104453","url":null,"abstract":"<p><p>Phosphatidylethanolamine (PE) is a major phospholipid in biological membranes and plays essential roles in autophagy, cell signaling, protein function, and membrane integrity. Its dynamic, conical structure supports membrane fluidity and curvature, which are crucial for processes such as signaling, autophagosome formation, membrane fusion, vesicle trafficking, and proper protein folding. Although PE is abundant, its significance for human health and disease has only recently come to light. Altered PE levels or disruptions in its metabolism have been associated with various conditions, including metabolic disorders such as non-alcoholic fatty liver disease (NAFLD), neurodegenerative diseases like Alzheimer's and Parkinson's, and several cancers. PE is synthesized primarily via two pathways: the CDP-ethanolamine (Kennedy) pathway and the mitochondrial phosphatidylserine decarboxylase (PSD) pathway, both of which are critical for maintaining lipid homeostasis. Advances in lipidomics now allow comprehensive profiling of PE species, facilitating the identification of disease-specific lipid biomarkers. This review expands current knowledge on the physiological roles of PE and elucidates mechanisms underlying PErelated lipid dysregulation in human disease.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell Sequencing Reveals Key Biological Insights into Intervertebral Disc Development and Degeneration.","authors":"Chaorong Yu, Wei Yang, Yanyan Wang, Yujie Zhang","doi":"10.2174/0115665240418547251215053012","DOIUrl":"https://doi.org/10.2174/0115665240418547251215053012","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IDD) is a common spinal disease that imposes a significant economic burden on healthcare systems. Understanding the biological processes involved in IDD development and degeneration is critical for developing potential therapeutic approaches. Single-cell RNA sequencing (scRNAseq) technology has revolutionized our understanding of cellular heterogeneity at the single-cell level and provided profound insights into the transcriptional landscape of IDD. This review provides an overview of research progress on the cellular biological characteristics of IDD occurrence and degeneration using scRNA-seq. It systematically summarizes the applications and key findings of scRNA-seq in subtyping cell populations, detecting transcriptomic changes, regulating signaling pathways, and elucidating cell-cell interactions in IDD. Additionally, it emphasizes the potential role of scRNA-seq in maintaining and repairing intervertebral disc tissues, from both preventive and therapeutic perspectives. In summary, this study underscores the extensive application of scRNA-seq in degenerative disc research and provides a foundation for future investigations and potential treatment strategies.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}