IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-01-28 DOI: 10.1080/13510002.2025.2455914

Lixuan Chen, Yingnan Wu, Tiying Lv, Rui Tuo, Yang Xiao

{"title":"Mesenchymal stem cells enchanced by salidroside to inhibit ferroptosis and improve premature ovarian insufficiency via Keap1/Nrf2/GPX4 signaling.","authors":"Lixuan Chen, Yingnan Wu, Tiying Lv, Rui Tuo, Yang Xiao","doi":"10.1080/13510002.2025.2455914","DOIUrl":"10.1080/13510002.2025.2455914","url":null,"abstract":"Background: Regenerative medicine researches have shown that mesenchymal stem cells (MSCs) may be an effective treatment method for premature ovarian insufficiency (POI). However, the efficacy of MSCs is still limited.Purpose: This study aims to explain whether salidroside and MSCs combination is a therapeutic strategy to POI and to explore salidroside-enhanced MSCs inhibiting ferroptosis via Keap1/Nrf2/GPX4 signaling.Methods: The effect of salidroside and MSCs on ovarian granular cells (GCs) was analyzed. After treatment, hormone levels and -fertility of rats were measured. Lipid peroxidation levels, iron deposition and mitochondrial morphology were detected. The genes and proteins of Keap1/Nrf2/GPX4 signaling were examined.Results: Salidroside and MSCs were found to inhibit cell death of GCs by reducing peroxidation and intracellular ferrous. Salidroside promotes the proliferation of MSCs and supports cell survival in ovary. Salidroside combined with MSCs therapy restored ovarian function, which was better than MSCs monotherapy. Salidroside-enhanced MSCs to inhibit ferroptosis. The results showed activation of the Keap1/Nrf2/GPX4 signaling and an increase in anti-ferroptosis molecule.Conclusions: Salidroside-enhanced MSCs as a ferroptosis inhibitor and provide new therapeutic strategies for POI. The possible mechanisms of MSCs were related to maintaining redox homeostasis via a Keap1/Nrf2/GPX4 signaling.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2455914"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11776066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143060219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Artemisinin protected human bronchial epithelial cells from amiodarone-induced oxidative damage via 5'-AMP-activated protein kinase (AMPK) activation. 青蒿素通过激活5′- amp活化蛋白激酶（AMPK）保护人支气管上皮细胞免受胺碘酮诱导的氧化损伤。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-01-13 DOI: 10.1080/13510002.2024.2447721

Chao Yang, Wenjun Xiong, Jiayi Dong, Xia Zhao, Guang Liang, Wenhua Zheng

{"title":"Artemisinin protected human bronchial epithelial cells from amiodarone-induced oxidative damage via 5'-AMP-activated protein kinase (AMPK) activation.","authors":"Chao Yang, Wenjun Xiong, Jiayi Dong, Xia Zhao, Guang Liang, Wenhua Zheng","doi":"10.1080/13510002.2024.2447721","DOIUrl":"10.1080/13510002.2024.2447721","url":null,"abstract":"Background: Amiodarone, a common antiarrhythmic drug, is known for its severe side effects, including pulmonary toxicity, which involves oxidative stress and apoptosis. Artemisinin, an antimalarial drug, has shown cytoprotective properties by inhibiting oxidative stress and apoptosis. This study investigated the protective effects of artemisinin against amiodarone-induced toxicity in human bronchial epithelial cells (BEAS-2B) and mouse models.Results: In vitro experiments revealed that amiodarone decreased cell viability, increased LDH release, ROS generation, caspase 3 activation, and apoptosis in BEAS-2B cells. Artemisinin counteracted these effects by upregulating p-AMPK, CaMKK2, Nrf2, and SOD1 protein levels, thereby protecting the cells from oxidative damage. The protective effect of artemisinin was diminished by the AMPK inhibitor Compound C or AMPKα knockdown. In vivo experiments demonstrated that artemisinin increased p-AMPK and Nrf2 protein levels in lung tissues, protecting against amiodarone-induced apoptosis and bronchial epithelial cell shedding in mice.Conclusion: These findings suggest that artemisinin protects airway epithelial cells and lung tissue from amiodarone-induced oxidative stress and apoptosis through AMPK activation, offering potential new strategies for preventing and treating amiodarone-induced pulmonary toxicity.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2447721"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11731350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Porphyromonas gulae and canine periodontal disease: Current understanding and future directions. 古卟啉单胞菌与犬牙周病：目前的认识和未来的方向。

IF 5.5 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-01-21 DOI: 10.1080/21505594.2024.2449019

Kyu Hwan Kwack, Eun-Young Jang, Cheul Kim, Young-Suk Choi, Jae-Hyung Lee, Ji-Hoi Moon

{"title":"Porphyromonas gulae and canine periodontal disease: Current understanding and future directions.","authors":"Kyu Hwan Kwack, Eun-Young Jang, Cheul Kim, Young-Suk Choi, Jae-Hyung Lee, Ji-Hoi Moon","doi":"10.1080/21505594.2024.2449019","DOIUrl":"10.1080/21505594.2024.2449019","url":null,"abstract":"Porphyromonas gulae has emerged as a notable pathogen in canine periodontal disease, akin to Porphyromonas gingivalis in human periodontitis. This review examines the initial isolation, phylogenetic analysis, habitat, host range, relationships with host health status and age, and key pathogenic determinants, including fimbriae, proteases, citrullinating enzyme, and lipopolysaccharide. Control strategies discussed include polyphosphate to disrupt haeme/iron utilization, clindamycin with interferon alpha to reduce bacterial load and enhance the immune response, and a protease inhibitor. Further research is needed to understand strain-level diversity of virulence factors and interactions between P. gulae and other oral bacteria, particularly Fusobacterium nucleatum, a common pathogen in both dogs and humans. The potential for interspecies transmission between dogs and humans warrants further research into these interactions. Extensive in vivo studies across various breeds are crucial to validate the effectiveness of proposed treatment strategies. This review emphasizes P. gulae's role in periodontal health and disease, setting the stage for future research and improved management of canine periodontal disease.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2449019"},"PeriodicalIF":5.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11756583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Activation of the mitochondrial unfolded protein response regulates the dynamic formation of stress granules. 线粒体未折叠蛋白反应的激活调节应激颗粒的动态形成。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-05-01 Epub Date: 2024-12-05 DOI: 10.1242/jcs.263548

Marta Lopez-Nieto, Zhaozhi Sun, Emily Relton, Rahme Safakli, Brian D Freibaum, J Paul Taylor, Alessia Ruggieri, Ioannis Smyrnias, Nicolas Locker

{"title":"Activation of the mitochondrial unfolded protein response regulates the dynamic formation of stress granules.","authors":"Marta Lopez-Nieto, Zhaozhi Sun, Emily Relton, Rahme Safakli, Brian D Freibaum, J Paul Taylor, Alessia Ruggieri, Ioannis Smyrnias, Nicolas Locker","doi":"10.1242/jcs.263548","DOIUrl":"10.1242/jcs.263548","url":null,"abstract":"To rapidly adapt to harmful changes to their environment, cells activate the integrated stress response (ISR). This results in an adaptive transcriptional and translational rewiring, and the formation of biomolecular condensates named stress granules (SGs), to resolve stress. In addition to this first line of defence, the mitochondrial unfolded protein response (UPRmt) activates a specific transcriptional programme to maintain mitochondrial homeostasis. We present evidence that the SG formation and UPRmt pathways are intertwined and communicate. UPRmt induction results in eIF2α phosphorylation and the initial and transient formation of SGs, which subsequently disassemble. The induction of GADD34 (also known as PPP1R15A) during late UPRmt protects cells from prolonged stress by impairing further assembly of SGs. Furthermore, mitochondrial functions and cellular survival are enhanced during UPRmt activation when SGs are absent, suggesting that UPRmt-induced SGs have an adverse effect on mitochondrial homeostasis. These findings point to a novel crosstalk between SGs and the UPRmt that might contribute to restoring mitochondrial functions under stressful conditions.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142501119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Fis1 regulates mitochondrial morphology, bioenergetics and removal of mitochondrial DNA damage in irradiated glioblastoma cells. Fis1调节辐照胶质母细胞瘤细胞的线粒体形态、生物能量学和mtDNA损伤的去除。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-05-01 Epub Date: 2025-01-28 DOI: 10.1242/jcs.263459

Yuli Buckley, Maria S K Stoll, Charles L Hoppel, Jason A Mears

{"title":"Fis1 regulates mitochondrial morphology, bioenergetics and removal of mitochondrial DNA damage in irradiated glioblastoma cells.","authors":"Yuli Buckley, Maria S K Stoll, Charles L Hoppel, Jason A Mears","doi":"10.1242/jcs.263459","DOIUrl":"10.1242/jcs.263459","url":null,"abstract":"In response to external stress, mitochondrial dynamics is often disrupted, but the associated physiologic changes are often uncharacterized. In many cancers, including glioblastoma (GBM), mitochondrial dysfunction has been observed. Understanding how mitochondrial dynamics and physiology contribute to treatment resistance will lead to more targeted and effective therapeutics. This study aims to uncover how mitochondria in GBM cells adapt to and resist ionizing radiation (IR), a component of the standard of care for GBM. Using several approaches, we investigated how mitochondrial dynamics and physiology adapt to radiation stress, and we uncover a novel role for Fis1, a pro-fission protein, in regulating the stress response through mitochondrial DNA (mtDNA) maintenance and altered mitochondrial bioenergetics. Importantly, our data demonstrate that increased fission in response to IR leads to removal of mtDNA damage and more efficient oxygen consumption through altered electron transport chain (ETC) activities in intact mitochondria. These findings demonstrate a key role for Fis1 in targeting damaged mtDNA for degradation and regulating mitochondrial bioenergetics through altered dynamics.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Translation of unspliced retroviral genomic RNA in the host cell is regulated in both space and time. 宿主细胞中未剪接的逆转录病毒基因组 RNA 的翻译在空间和时间上都受到调控。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-04-07 Epub Date: 2025-01-27 DOI: 10.1083/jcb.202405075

Felipe Leon-Diaz, Célia Chamontin, Sébastien Lainé, Marius Socol, Edouard Bertrand, Marylène Mougel

引用次数: 0

Arginylation of ⍺-tubulin at E77 regulates microtubule dynamics via MAP1S.

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-04-07 Epub Date: 2025-01-24 DOI: 10.1083/jcb.202406099

Brittany MacTaggart, Junling Wang, Hsin-Yao Tang, Anna Kashina

{"title":"Arginylation of ⍺-tubulin at E77 regulates microtubule dynamics via MAP1S.","authors":"Brittany MacTaggart, Junling Wang, Hsin-Yao Tang, Anna Kashina","doi":"10.1083/jcb.202406099","DOIUrl":"10.1083/jcb.202406099","url":null,"abstract":"Arginylation is the posttranslational addition of arginine to a protein by arginyltransferase-1 (ATE1). Previous studies have found that ATE1 targets multiple cytoskeletal proteins, and Ate1 deletion causes cytoskeletal defects, including reduced cell motility and adhesion. Some of these defects have been linked to actin arginylation, but the role of other arginylated cytoskeletal proteins has not been studied. Here, we characterize tubulin arginylation and its role in the microtubule cytoskeleton. We identify ATE1-dependent arginylation of ⍺-tubulin at E77. Ate1-/- cells and cells overexpressing non-arginylatable ⍺-tubulinE77A both show a reduced microtubule growth rate and increased microtubule stability. Additionally, they show an increase in the fraction of the stabilizing protein MAP1S associated with microtubules, suggesting that E77 arginylation directly regulates MAP1S binding. Knockdown of Map1s is sufficient to rescue microtubule growth rate and stability to wild-type levels. Together, these results demonstrate a new type of tubulin regulation by posttranslational arginylation, which modulates microtubule growth rate and stability through the microtubule-associated protein, MAP1S.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 4","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11775831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033038","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}

引用次数: 0

Rectification of planar orientation angle switches behavior and replenishes contractile junctions.

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-04-03 Epub Date: 2025-01-23 DOI: 10.1083/jcb.202309069

Katie Linvill, Liam J Russell, Timothy E Vanderleest, Hui Miao, Yi Xie, J Todd Blankenship, Dinah Loerke

{"title":"Rectification of planar orientation angle switches behavior and replenishes contractile junctions.","authors":"Katie Linvill, Liam J Russell, Timothy E Vanderleest, Hui Miao, Yi Xie, J Todd Blankenship, Dinah Loerke","doi":"10.1083/jcb.202309069","DOIUrl":"10.1083/jcb.202309069","url":null,"abstract":"In the early Drosophila embryo, germband elongation is driven by oriented cell intercalation through t1 transitions, where vertical (dorsal-ventral aligned) interfaces contract and then resolve into new horizontal (anterior-posterior aligned) interfaces. Here, we show that contractile events produce a continuous \"rectification\" of cell interfaces, in which interfaces systematically rotate toward more vertical orientations. As interfaces rotate, their behavior transitions from elongating to contractile regimes, indicating that the planar polarized identities of cell-cell interfaces are continuously re-interpreted in time depending on their orientation angle. Rotating interfaces acquire higher levels of Myosin II motor proteins as they become more vertical, while disruptions to the contractile molecular machinery reduce the rates of rotation. Through this angle rectification, the available pool of contractile interfaces is continuously replenished, as new interfaces acquire a contractile identity through rotation. Thus, individual cells acquire additional interfaces that are capable of undergoing t1 transitions, allowing cells to participate in multiple staggered rounds of intercalation events.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 4","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11756375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023645","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}

引用次数: 0

VPS41 recruits biosynthetic LAMP-positive vesicles through interaction with Arl8b.

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-04-03 Epub Date: 2025-02-05 DOI: 10.1083/jcb.202405002

Paolo Sanzà, Jan van der Beek, Derk Draper, Cecilia de Heus, Tineke Veenendaal, Corlinda Ten Brink, Ginny G Farías, Nalan Liv, Judith Klumperman

{"title":"VPS41 recruits biosynthetic LAMP-positive vesicles through interaction with Arl8b.","authors":"Paolo Sanzà, Jan van der Beek, Derk Draper, Cecilia de Heus, Tineke Veenendaal, Corlinda Ten Brink, Ginny G Farías, Nalan Liv, Judith Klumperman","doi":"10.1083/jcb.202405002","DOIUrl":"https://doi.org/10.1083/jcb.202405002","url":null,"abstract":"Vacuolar protein sorting 41 (VPS41), a component of the homotypic fusion and protein sorting (HOPS) complex for lysosomal fusion, is essential for the trafficking of lysosomal membrane proteins via lysosome-associated membrane protein (LAMP) carriers from the trans-Golgi network (TGN) to endo/lysosomes. However, the molecular mechanisms underlying this pathway and VPS41's role herein remain poorly understood. Here, we investigated the effects of ectopically localizing VPS41 to mitochondria on LAMP distribution. Using electron microscopy, we identified that mitochondrial-localized VPS41 recruited LAMP1- and LAMP2A-positive vesicles resembling LAMP carriers. The retention using selective hooks (RUSH) system further revealed that newly synthesized LAMPs were specifically recruited by mitochondrial VPS41, a function not shared by other HOPS subunits. Notably, we identified the small GTPase Arl8b as a critical factor for LAMP carrier trafficking. Arl8b was present on LAMP carriers and bound to the WD40 domain of VPS41, enabling their recruitment. These findings reveal a unique role of VPS41 in recruiting TGN-derived LAMP carriers and expand our understanding of VPS41-Arl8b interactions beyond endosome-lysosome fusion, providing new insights into lysosomal trafficking mechanisms.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 4","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Expression and role of CTHRC1 in inflammatory bowel disease in children.

IF 2 4区生物学

Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-01-25 DOI: 10.1007/s10616-025-00705-x

Heng Tang, Xiang Gao, Zhaofang Wu, Jia Chen, Li Chen, Xiang Du

{"title":"Expression and role of CTHRC1 in inflammatory bowel disease in children.","authors":"Heng Tang, Xiang Gao, Zhaofang Wu, Jia Chen, Li Chen, Xiang Du","doi":"10.1007/s10616-025-00705-x","DOIUrl":"10.1007/s10616-025-00705-x","url":null,"abstract":"Inflammatory bowel disease (IBD) is a chronic, progressive, immune-mediated, gastrointestinal inflammatory disease with increasing occurrences in children. Collagen triple helix repeat containing 1 (CTHRC1), a migration-promoting protein, acts as a tumor-promoting factor in malignant tumors. However, functions and mechanisms of CTHRC1 in children with IBD remain unclear. This study aimed to determine the effects and mechanisms of CTHRC1 on dextran sodium sulfate (DSS)-treated HT-29 cells. HT-29 control cells were exposed to 2% DSS to develop an in vitro IBD model. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting were used to assess CTHRC1 expression in serum of children with IBD and HT-29 cells. Cell viability and apoptosis were assessed using MTT and flow cytometry (FCM). Expressions of cleaved-Caspase3 and Caspase3 were determined by western blotting. The cytokine production (TNF-α, IL-1β and IL-6) in HT-29 cells was measured by ELISA assay. Activation or inactivation of NF-κB signaling pathway was confirmed by western blot assay. Results showed that CTHRC1 expression was upregulated in the IBD serum and HT-29 control cells. The level of CTHRC1 was lower in CTHRC1-siRNA transfected cells than in control siRNA-treated cells. Notably, silence of CTHRC1 markedly enhanced HT-29 cells viability, decreased apoptotic cells, suppressed cleaved-Caspase3 expression, inhibited cleaved-Caspase3/Caspase3 ratio, reduced the production of inflammatory cytokines, and blocked NF-κB signaling pathway induced by DSS. However, these effects were reversed following diprovocim treatment. Thus, that knockdown of CTHRC1 alleviated DSS-induced HT-29 cell injury by inhibiting the NF-κB signaling pathway in vitro, providing a new therapeutic target for IBD in children.Supplementary information: The online version contains supplementary material available at 10.1007/s10616-025-00705-x.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"44"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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