Cell Proliferation最新文献

{"title":"MD-1 Deficiency Mitigates Atherosclerosis by Inhibiting NLRP3 Inflammasome Activation via cGAS-STING Dependent Pathway in Macrophages.","authors":"Fang Zhao, Zhili Jin, Zhiwei Cai, Quan Zhang, Tao He, Xiangjie Kong, Ming Chen, Zhibing Lu, Xiaorong Hu, Wen-Lin Cheng","doi":"10.1111/cpr.70288","DOIUrl":"10.1111/cpr.70288","url":null,"abstract":"<p><p>MD-1 plays significant roles in various pathological processes closely associated with cardiovascular diseases through its functions in different cell types. However, the critical effects and molecular mechanisms mediated by MD-1 in macrophages involved in the development of atherosclerosis remain elusive. In this study, we observed that the expression of MD-1 was upregulated in atherosclerotic plaques derived from human carotid arteries, as analysed through the Gene Expression Omnibus database. Additionally, MD-1 expression was elevated in the aortas of hyperlipidemic ApoE-deficient mice and in oxidised low-density lipoprotein-stimulated bone marrow-derived macrophages, as demonstrated by RT-PCR and western blot analyses. Furthermore, MD-1 expression exhibited strong co-localisation with macrophages, as confirmed by double immunofluorescence staining. Notably, MD-1^-/-ApoE^-/- mice subjected to a high-fat diet displayed a significant reduction in atherosclerotic plaques throughout the entire aorta, aortic root, and brachiocephalic arteries. Moreover, the plaques in MD-1^-/-ApoE^-/- mice were more stable, characterised by a decreased necrotic core size, reduced macrophage infiltration, and lower lipid deposition, alongside an increased accumulation of collagen and smooth muscle cells. Bone marrow transplantation from MD-1^-/-ApoE^-/- mice to ApoE^-/- mice markedly attenuated the development of atherosclerosis. This attenuation was associated with an enhanced anti-inflammatory macrophage phenotype and a reduction in pro-inflammatory macrophage polarisation. Similar effects of MD-1 ablation on macrophage behaviour were also observed in vitro. Mechanistically, MD-1 deficiency inhibited the cyclic GMP-AMP synthase-stimulator of interferon genes-TANK-binding kinase 1-IRF3 pathway, thereby attenuating NLRP3 inflammasome activation in macrophages. However, the use of the STING agonist DMXAA counteracted the effects of MD-1 deficiency on macrophage polarisation. Our findings reveal MD-1 promotes pro-inflammatory (M1-like) macrophage polarisation in atherosclerosis by inhibiting NLRP3 inflammasome activation via a cGAS-STING dependent pathway. These results suggest that MD-1 neutralisation could be a potential therapeutic strategy for atherosclerosis management.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":" ","pages":"e70288"},"PeriodicalIF":7.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664726/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Comprehensive Comparative Analysis of Sequence-Based Deep Learning Models for Single-Cell Genomics","authors":"Guoxia Wen,&nbsp;Jiaqi Li,&nbsp;Hanyu Wu,&nbsp;Jialing Fang,&nbsp;Yuting Fu,&nbsp;Mengmeng Jiang,&nbsp;Yuqing Mei,&nbsp;Rui Xu,&nbsp;Yuxuan Du,&nbsp;Siran Chu,&nbsp;Guoji Guo,&nbsp;Xiaoping Han,&nbsp;Jingjing Wang","doi":"10.1111/cpr.70274","DOIUrl":"10.1111/cpr.70274","url":null,"abstract":"<p>To streamline the application of sequence-based DL methods in single-cell genomics, we established a two-layer CNN as our baseline model. We focus our benchmark on how data characteristics, hyperparameter optimization, and advanced model architectures impact performance across sequence-to-expression and sequence-to-regulation tasks. A key contribution of our study is the exploration of multi-task learning (MTL) frameworks for mitigate technical sparsity. We demonstrated that MTL significantly enhances the modeling of cellular heterogeneity, evaluating the effectiveness of task grouping and balancing strategies, with particular focus on the prediction of rare cell types. Our comprehensive comparative analysis provided an actionable framework and valuable insights for guiding future research endeavors and facilitating the development of the sequence-based DL models capable of superior predictive performance in single-cell genomics.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 10","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13500174/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148807821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High Uric Acid Promotes Stem Leydig Cell Senescence by CCDC90B Mediates Mitochondrial Quality Control Imbalance","authors":"Jiayu Huang,&nbsp;Ao Wang,&nbsp;Xiangyu Li,&nbsp;Peng Huang,&nbsp;Kaixuan Zeng,&nbsp;Lu Sun,&nbsp;Moxuan Li,&nbsp;Yixiang Chen,&nbsp;Jiancheng Wang","doi":"10.1111/cpr.70237","DOIUrl":"10.1111/cpr.70237","url":null,"abstract":"<p>Hyperuricemia is a common metabolic disease and an important risk factor for low testosterone levels in men. The functional homeostasis of stem Leydig cells (SLCs) is crucial for maintaining testosterone levels. However, the potential molecular mechanism of how high uric acid (UA) levels affect SLC function remains to be elucidated. Here, we reveal that at the single-cell RNA sequencing level, SLCs exhibit senescence under high UA conditions. Mechanistically, UA binds to CCDC90B, leading to its significant accumulation within cells. This exacerbates the influx of calcium ions into mitochondria, resulting in mitochondrial quality control (MQC) imbalance. In addition, at the level of organoids and transgenic mice, we observe SLC senescence is alleviated and considerable testosterone recovery after AAV8-CCDC90B treatment. In summary, these results indicate that SLC senescence under high UA is regulated in a MQC-dependent manner, with CCDC90B being a key regulatory target. Meanwhile, AAV-mediated gene therapy may offer a promising therapeutic approach for patients with low testosterone levels.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 10","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13325638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Localised Autophagy Inhibition by Nanodiamonds Potentiates Arsenic Therapy With Favourable Safety Profile in Solid Tumours","authors":"Yiliu Wang,&nbsp;Zhifen Cui,&nbsp;Jichao Zhang,&nbsp;Shitai Zhu,&nbsp;Linjie Guo,&nbsp;Qisheng Wang,&nbsp;Ying Zhu,&nbsp;Shihua Luo,&nbsp;Huating Kong","doi":"10.1111/cpr.70234","DOIUrl":"10.1111/cpr.70234","url":null,"abstract":"<p>Arsenic trioxide (ATO) shows limited efficacy against solid tumours, largely because it induces protective autophagy that attenuates its pro-apoptotic activity. Our previous studies established that nanodiamonds (NDs) function as nanoparticle autophagy inhibitors (NAPIs) when delivered systemically, markedly enhancing ATO efficacy in orthotopic liver tumour models by blocking NUPR1-mediated autolysosomal clearance. However, systemic administration remains inefficient in modulating the local autophagic microenvironment within tumours. Here we developed an interventional strategy based on intratumoral injection to assess the feasibility and biosafety of locally blocking autophagic flux while substantially reducing the required ATO dosage, thereby maximising the synergistic anti-tumour effects of NDs and ATO. In HepG2 hepatocellular carcinoma cells, NDs markedly blocked the late stage of autophagic flux, thereby significantly amplifying ATO-induced apoptosis. In a subcutaneous xenograft liver cancer mouse model, intratumoral co-administration of NDs with low-dose ATO achieved ~91% tumour inhibition and effectively eliminated the systemic toxicity associated with high-dose ATO monotherapy. Notably, the synergistic antitumor effect was independent of increased intratumoral ATO accumulation and was driven instead by targeted modulation of the autophagic pathway. Collectively, this study demonstrates a mechanism of localised, nanomaterial-mediated autophagy regulation and offers an efficient, safe strategy for interventional therapy of advanced solid tumours.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 10","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13325723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147970704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of Ornithine Decarboxylase 1 Mitigates Denervation-Induced Muscle Atrophy by Suppressing Proteolysis and Preserving Muscle Stem Cell Homeostasis","authors":"Mingming Zhang,&nbsp;Feifan Chang,&nbsp;Siliang Ge,&nbsp;Fuming Cao,&nbsp;Pincong Fu,&nbsp;Haobo Zhang,&nbsp;Ming Chen,&nbsp;Yi Li,&nbsp;Peifu Tang,&nbsp;Pengbin Yin","doi":"10.1111/cpr.70231","DOIUrl":"10.1111/cpr.70231","url":null,"abstract":"<p>Neural innervation is of vital importance for muscle mass and function, and denervation induces progressive muscle atrophy, which lacks effective treatments. Polyamine metabolism is reported to be innervation responsive and involved in denervation-induced muscle atrophy, yet the effects of polyamine in denervated muscle atrophy remain unknown. In this study, using a sciatic nerve transection model, we observed progressive increases in putrescine and spermidine, alongside induction of polyamine metabolism enzymes, coincident with the early rapid atrophy phase post denervation. Pharmacological ODC1 inhibition lowered intramuscular polyamines and improved denervated muscle atrophy and fibrosis. In contrast, spermidine supplementation induced muscle atrophy and atrogene expression in healthy and denervated muscle, implicating spermidine as a pro-atrophic metabolite. Single-nucleus sequencing revealed an expansion of atrophic myonuclei and depletion of type IIb myonuclei post denervation. DFMO reduced the atrophic myonuclear fraction, increased MuSCs abundance, and suppressed FAPs derived FGF signalling dominated by the Fgf7-Fgfr2 axis to maintain MuSCs homeostasis. Taken together, our results demonstrate that dysregulated polyamine metabolism is a key contributor to denervation-induced muscle atrophy, and ODC1 inhibition mitigates muscle atrophy and fibrosis by restraining proteolysis and preserving MuSCs homeostasis, which will provide references for future clinical treatments.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 10","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13325653/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147947824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Noncanonical Protein Degradation Pathway That Regulates Germ Cell Maintenance","authors":"Meng Liu,&nbsp;Xiya Qiu,&nbsp;Wenying Qu,&nbsp;Yue Ma,&nbsp;Mingyuan Bao,&nbsp;Yuxuan Feng,&nbsp;Xiaochu Wang,&nbsp;Tao Zhou,&nbsp;Bo Zheng,&nbsp;Shunyu Hou,&nbsp;Yu Xia,&nbsp;Qingxia Meng","doi":"10.1111/cpr.70259","DOIUrl":"10.1111/cpr.70259","url":null,"abstract":"<p>SENP8 regulates a non-canonical NEDD8-dependent pathway to stabilize STAT1, promote CCL2/CCL5 transcription, and maintain germ cell proliferation and migration.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 10","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13370090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148444707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suppression of Retinal Neovascularisation by Tetrahedral Framework Nucleic Acids-Resveratrol Via Dual Anti-Angiogenesis and Anti-Inflammation","authors":"Yili Jin,&nbsp;Tao Cai,&nbsp;Junyang Huang,&nbsp;Li Chen,&nbsp;Yi Lin,&nbsp;Jingying Liu,&nbsp;You Wang,&nbsp;Xiaoyan Ding","doi":"10.1111/cpr.70227","DOIUrl":"10.1111/cpr.70227","url":null,"abstract":"<p>Retinal neovascular diseases, such as retinopathy of prematurity and diabetic retinopathy, threaten vision by disrupting retinal structure and function through pathological neovascularisation and chronic inflammation. Existing anti-VEGF therapies primarily target angiogenesis, offering limited control over inflammation and requiring repeated administration. Here, we developed a resveratrol (RSV)-loaded tetrahedral framework nucleic acid nanostructure (tFNAs-RSV) to achieve concurrent anti-angiogenic and anti-inflammatory effects. tFNAs provided a biocompatible, stable and penetration-efficient carrier that enhanced RSV ocular delivery and bioactivity. In hypoxia-induced retinal neovascularisation models, tFNAs-RSV markedly reduced neovascular lesion area, vascular leakage and retinal inflammatory cell infiltration. Mechanistically, tFNAs-RSV suppressed HIF-1 signalling and inhibited the p38 MAPK pathway and NF-κB p65 pathway. Collectively, these results validate tFNAs-RSV as a promising nanoplatform for treating retinal neovascular diseases, with an emphasis on inhibiting neovascularisation and inflammation.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 10","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13325993/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zeb2 Controls Retinal Physiological and Pathological Angiogenesis by Regulating Astrocyte Proliferation and Differentiation","authors":"Jing Liu,&nbsp;Yanan Guo,&nbsp;Kangjian Xiang,&nbsp;Shuyi Wang,&nbsp;Dongchang Xiao,&nbsp;Mengqing Xiang","doi":"10.1111/cpr.70236","DOIUrl":"10.1111/cpr.70236","url":null,"abstract":"<p>Retinal angiogenesis relies on a precisely timed interaction between astrocytes and endothelial cells (ECs), yet the transcriptional regulatory program underlying this complex neurovascular crosstalk remains poorly characterized. Here, we define Zeb2 as a pivotal transcriptional modulator of retinal astrocyte function that coordinates developmental and pathological vascular growth. It is transiently expressed in retinal astrocyte progenitor cells during development and re-induced under pathological hypoxia. Conditional ablation of <i>Zeb2</i> in retinal astrocytes enhanced their proliferation, migration, and maturation by upregulating VEGFA and altering other signalling, leading to excessive superficial vascular growth during development. In oxygen-induced retinopathy, <i>Zeb2</i> inactivation exacerbated pathological neovascularization while impairing reparative revascularization, which is associated with a transcriptional signature favouring tuft ECs over tip ECs. Mechanistically, it inhibited the neurotoxic A1 astrocyte identity, resulting in dampened inflammatory response and diminished genetic program promoting revascularization and/or preventing neovascularization including Plxnd1, Nrf2, and FGF2 signalling. These findings establish Zeb2 as an oxygen-sensitive regulator of astrocyte function that differentially modulates physiological and pathological angiogenesis, highlighting its potential as a therapeutic target in proliferative retinopathies.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 10","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13325830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148027513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative Stress Drives Cell Cycle Stalling, Apoptosis and Metabolic Suppression in Cystatin B Deficient EPM1 Patient iPSCs","authors":"Shekhar Singh,&nbsp;Lidiia Plotnikova,&nbsp;Teemu Tiukuvaara,&nbsp;Reetta Kälviäinen,&nbsp;Riikka H. Hämäläinen","doi":"10.1111/cpr.70232","DOIUrl":"10.1111/cpr.70232","url":null,"abstract":"<p>Cystatin B (CSTB) is an inhibitor of cysteine proteases, particularly cathepsins. Biallelic loss-of-function mutations in the <i>CSTB</i> gene are causative for progressive myoclonic epilepsy type 1 (EPM1), a neurodegenerative disorder characterised by stimulus-sensitive myoclonus and generalised tonic–clonic seizures. Pathomechanisms underlying the disease progression include disturbed proteostasis, increased oxidative stress, neuroinflammation and increased neuronal apoptosis. CSTB downregulation can also lead to cell cycle defects and reduced cell proliferation. Conversely, overexpression of CSTB has been reported to drive proliferation and survival of cancer cells, emphasising the important role of CSTB in cell growth and survival. In the current study, we focused on the role of CSTB in regulating proliferation and survival of EPM1 patients' stem cells. We reprogrammed EPM1 patient fibroblasts into induced pluripotent stem cells (iPSCs), a highly proliferative cell type. Patient cells manifested poor growth and increased apoptosis. Further, EPM1 cells showed oxidative stress, increased lysosomal activity, increased DNA damage and suppressed metabolism. Treatment with antioxidants rescued the growth phenotype and activated metabolism, suggesting oxidative stress as the cause and suppressed metabolism as a protective response. Our data strengthen the central role of CSTB in supporting cell survival and growth. Elucidating the regulatory role of CSTB expression in cell growth can advance our understanding of the pathophysiological mechanisms underlying both EPM1 and cancer and could inform the development of novel therapeutic strategies.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 10","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13325810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147970760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Monocytes Derived From Human Pluripotent Stem Cells Engineered for Detection of Pyrogens","authors":"Jingjing Liu,&nbsp;Bingyu Cai,&nbsp;Tingting Gao,&nbsp;Wumei Wei,&nbsp;Liu Wang,&nbsp;Qi Zhou,&nbsp;Wei Li,&nbsp;Jie Hao,&nbsp;Jun Wu","doi":"10.1111/cpr.70233","DOIUrl":"10.1111/cpr.70233","url":null,"abstract":"<p>Pyrogens, including endotoxins and non-endotoxins, are key factors that impact the safety of parenterally administered drugs as contaminants. Currently, traditional pyrogen detection methods primarily rely on the Rabbit Pyrogen Test (RPT) and the Limulus Amebocyte Lysate (LAL) assay, both of which are derived from animal-based systems. However, both methods possess certain limitations. The RPT demonstrates lower reproducibility and a higher false-positive rate compared to the LAL assay; in contrast, the LAL test is limited to detecting endotoxins from Gram-negative organisms. The Monocyte Activation Test (MAT), which is based on monocytes, has emerged as the most promising alternative to traditional pyrogen detection methods. However, the MAT is operationally complex, time-consuming, and exhibits significant individual variability; it typically requires a substantial volume of human blood, thereby considerably limiting its practical application. To overcome these limitations, we developed a rapid pyrogen detection method based on monocytes derived from human embryonic stem cells (hESCs), integrated with a luciferase reporter system. By leveraging the stability and pluripotency of hESCs, we can obtain numerous hESC-derived monocytes (hESC-Mono) through directed in vitro differentiation. These hESC-Mono exhibit batch-to-batch consistency and closely resemble peripheral blood monocytes in functionality. We have demonstrated that hESC-Mono possess sensitive reporting capabilities for at least three types of pyrogens: lipopolysaccharide (LPS), a major component of the cell wall of Gram-negative bacteria; lipoteichoic acid (LTA), a key constituent of the cell wall of Gram-positive bacteria; and fungal Zymosan. Furthermore, we have confirmed that hESC-Mono maintain stable expression of Toll-like receptors, which are among the primary determinants of the reliable detection of pyrogens. Consequently, we have successfully developed and validated a novel pyrogen detection method based on the integration of an in vitro hPSC-directed differentiation system with a luciferase-based reporter assay, thereby offering a promising alternative to traditional pyrogen detection methods.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 10","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13325647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147980675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}