In Vitro Cellular & Developmental Biology. Animal最新文献

{"title":"Correction: The adaptation of bovine embryonic stem cells to the changes of feeder layers.","authors":"Wenqiang Xu, Lingna Gao, Wei Li, Jing Wang, Yongli Yue, Xueling Li","doi":"10.1007/s11626-024-01013-y","DOIUrl":"10.1007/s11626-024-01013-y","url":null,"abstract":"","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"486-491"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143803117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Establishment of a highly sensitive porcine alveolar macrophage cell line for African swine fever virus.","authors":"Xiangwan Lu, Xiadan Gong, Yingshuo Sun, Lang Gong, Yan Zhang","doi":"10.1007/s11626-025-01016-3","DOIUrl":"10.1007/s11626-025-01016-3","url":null,"abstract":"<p><p>African swine fever (ASF) caused by the African swine fever virus (ASFV) is a significant threat to domestic pig populations because of its highly contagious nature and associated morbidity and mortality. The lack of an appropriate cell line for ASFV propagation has significantly hindered the development of a safe and effective vaccine. In this study, we aimed to identify a cell line that is highly receptive to ASFV by evaluating various genes to determine their ability to support ASFV infection and replication. Our investigation revealed the efficient infection of a porcine alveolar macrophage cell line iPAM, upon stable overexpression of the transmembrane protein 107 (TMEM107). An isolated monoclonal cell line iPAM^{pCDH-TMEM107-B6} that was derived from the parental iPAM cell line exhibited increased susceptibility to ASFV infection. Notably, iPAM^{pCDH-TMEM107-B6} cells concurrently expressed ASFV B646L and ASFV p30 proteins after infection with ASFV. Biological characterization of iPAM^{pCDH-TMEM107-B6} revealed an enhanced proliferative capacity without compromised phagocytic function, indicating the retention of key cellular traits following genetic modification. The iPAM^{pCDH-TMEM107-B6} cell line has significant potential for ASFV research and will facilitate tasks such as isolation, replication, and genetic manipulation. The establishment of ASFV-sensitive cell lines provides an in vitro research platform for ASFV investigations, thereby advancing our understanding of the pathogenic mechanisms and aiding in vaccine development efforts.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"425-437"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SPARC: a key mediator of apoptosis in human umbilical vein endothelial cells and its role in hypertension mechanism.","authors":"Yingyue Zhang, Haijing Zhao, Liuyang Tian, Zengao Yang, Li Zheng, Honghong Zhang, Yue Zhu, Yuhan Ma, Yong Xu, Yuqi Liu","doi":"10.1007/s11626-025-01026-1","DOIUrl":"10.1007/s11626-025-01026-1","url":null,"abstract":"<p><p>Hypertensionis a leading global health issue associated with high mortality and severe complications. Understanding its molecular mechanisms is essential for identifying novel therapeutic targets. Secreted protein acidic and rich in cysteine (SPARC) is associated with cell migration, disease pathophysiology, and inflammation; however, its role in hypertension remains under investigation. This study investigates the role of SPARC in hypertension, focusing on its impact on endothelial dysfunction.Using the GSE75815 dataset from the GEO database, we identified 71 differentially expressed genes (DEGs) associated with hypertension. Pathway analyses and protein-protein interaction networks constructed through the STRING database highlighted six hub genes, with further evaluation based on Comparative Toxicogenomics Database (CTD) scores. Immune cell profiling via ImmuCellAI revealed an increase in naive B cells, positively correlating with hub gene expression.Experimental validation in human umbilical vein endothelial cells (HUVECs) treated with angiotensin II demonstrated that SPARC downregulation reduced apoptosis and BAX expression. Silencing SPARC enhanced endothelial cell proliferation, migration, and nitric oxide production, counteracting angiotensin II-induced damage. Notably, angiotensin II upregulated SPARC secretion, suggesting its critical role in mediating endothelial dysfunction.These findings establish SPARC as a key contributor to the molecular pathways underlying hypertension. Targeting SPARC may represent a novel therapeutic strategy to mitigate endothelial dysfunction and improve outcomes for hypertensive patients.Our findings highlight SPARC as a key player in the molecular pathways of hypertension. Modulating SPARC expression may offer a promising therapeutic strategy to counteract endothelial dysfunction and improve outcomes in hypertensive patients.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"374-388"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpression of miR-20a targeting DUSP3 inhibits OCLN ubiquitination levels and alleviates sepsis induced intestinal barrier dysfunction.","authors":"Liming Cheng, Bo Feng, Chao Xie, Chunyan Chen, Linghui Guo","doi":"10.1007/s11626-025-01052-z","DOIUrl":"10.1007/s11626-025-01052-z","url":null,"abstract":"<p><p>Sepsis is a severe organ dysfunction syndrome caused by the host's dysfunctional response to infection. Sepsis can severely damage intestinal epithelial tissue, lead to intestinal barrier dysfunction, and seriously endanger human health. Therefore, this study aimed to explore the mechanism of miR-20a in sepsis-induced intestinal barrier dysfunction. In this study, mice and NCM460 cells were subjected to cecal ligation and puncture (CLP) and 1 μg/mL LPS, respectively, to establish a sepsis model. The expression of relevant genes, apoptosis, inflammation, and intestinal barrier dysfunction-related indices under the conditions of overexpression of miR-20a or DUSP3 and knockdown of DUSP3 or OCLN were assessed by western blotting, RT-qPCR, ELISA, flow cytometry, immunofluorescence, and HE staining. The experimental results revealed that in sepsis-induced intestinal barrier dysfunction, the expression of miR-20a and OCLN was downregulated, whereas that of DUSP3 was upregulated. Functionally, miR-20a inhibited LPS-induced intestinal epithelial cell apoptosis and inflammation and relieved sepsis-induced intestinal barrier dysfunction in mice. Experiments investigating the downstream mechanisms revealed that miR-20a overexpression suppressed LPS-induced intestinal epithelial cell apoptosis and inflammation and relieved sepsis-induced intestinal barrier dysfunction by targeting and inhibiting DUSP3 levels and OCLN ubiquitination. In conclusion, miR-20a relieves sepsis-induced intestinal barrier dysfunction by inhibiting DUSP3 and suppressing the ubiquitination of OCLN.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"459-471"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA PVT1 promotes proliferation and migration in gallbladder adenocarcinoma by modulating miR-2355-5p/AGO1 axis.","authors":"Dong Liu, He Wang, Jun Fang, Jialin Luo, Ke Lu, Guan Liu, Luying Liu","doi":"10.1007/s11626-025-01025-2","DOIUrl":"10.1007/s11626-025-01025-2","url":null,"abstract":"<p><p>To investigate how lncRNA plasmacytoma variant translocation 1 (PVT1) contributed to the pathogenesis of gallbladder adenocarcinoma (GBA). Bioinformatics techniques were used to analyze differentially expressed lncRNA, and downstream miRNA and mRNA were identified using databases. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting were utilized to analyze the RNA and protein expressions in different cells. The binding relationships between different genes were confirmed utilizing luciferase assay and RNA Immunoprecipitation (RIP) assay. Cell growth and migration were examined through CCK-8, colony formation, and Transwell assays. Several in vivo experiments were utilized to determine how the PVT1/miR-2355-5p/AGO1 pathway on tumor growth. Elevated PVT1 was observed in GBA cells, which may further aggravate cell malignant properties. Based on bioinformatics analysis, an interaction between miR-2355-5p and either PVT1 or AGO1 was identified, which was confirmed utilizing dual luciferase reporter assays and RIP assays. Silencing PVT1 (si-PVT1) led to a reduction in AGO1 expression, while depletion of miR-2355-5p reversed this effect. In vivo, PVT1 knockdown significantly inhibited tumor growth, an effect that was reversed by miR-2355-5p downregulation. This study showed that PVT1 facilitated GBA progression via the modulation of the miR-2355-5p/AGO1 axis. These findings underscored the potential therapeutic significance of targeting the lncRNA PVT1 in the treatment of GBA.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"403-415"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144008888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-lung cancer activity of lotusine in non-small cell lung cancer HCC827 via reducing proliferation, oxidative stress, induction of apoptosis, and G0/G1 cell cycle arrest via suppressing EGFR-Akt-ERK signalling.","authors":"Yuanmin Lan, Jing Sun, Jiqing Xu, Xiaoying Chen","doi":"10.1007/s11626-025-01048-9","DOIUrl":"10.1007/s11626-025-01048-9","url":null,"abstract":"<p><p>Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related deaths worldwide, with resistance to targeted therapies and the need for novel therapeutic agents driving ongoing research. In this study, we investigated the anti-lung cancer activity of lotusine, a natural alkaloid, in the A549 (non-EGFR mutant), and EGFR-mutant HCC827 NSCLC cell line (deletion in exon 19). Our results demonstrated that lotusine significantly inhibited cell proliferation in a concentration- and time-dependent manner of HCC827 cells in comparison to A549 cells. Mechanistic analysis revealed that lotusine induced apoptosis in HCC827 cells, as evidenced by increased expression of pro-apoptotic markers (Bax and cleaved caspase-3) and decreased levels of anti-apoptotic proteins (Bcl-2). Cell cycle analysis indicated that lotusine caused G0/G1 phase arrest. Importantly, lotusine exerted its effects through the inhibition of the epidermal growth factor receptor (EGFR) EGFR-Akt-ERK signaling pathway, as evidenced by reduction of p-EGFR, p-Akt, and p-ERK in a western blot analysis in HCC827 cells. These findings suggest that lotusine exerts potent anti-cancer effects via a multifaceted mechanism, including inhibition of proliferation, apoptosis induction, and cell cycle arrest, predominantly mediated by EGFR suppression. This study highlights lotusine as a promising therapeutic candidate for the treatment of EGFR-mutant NSCLC and provides insights into its molecular mechanisms of action, paving the way for further preclinical and clinical evaluations.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"450-458"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory effects of carbohydrazide indole derivative on micro-blood vessel growth using ex vivo, in vivo, and in vitro assays.","authors":"Bayan Jamal Khaleel, Hayder Ridha-Salman, Haitham Mahmood Kadhim, Omeed M Hassan, Ammar Kubba, Hayder B Sahib","doi":"10.1007/s11626-025-01019-0","DOIUrl":"https://doi.org/10.1007/s11626-025-01019-0","url":null,"abstract":"<p><p>Defective angiogenesis is a characteristic of many diseases, notably cancer and immune-mediated conditions. Numerous shortcomings in anti-angiogenic therapies, including undesirable effects, drug resistance, and cancer recurrence, encouraged the development of innovative medicines with improved anti-angiogenic efficacy. Indole analogues are thought to interact with the mitotic spindle, preventing malignant human cells from multiplying and invading. N'-(1-Benzyl-2-oxoindolin-3-ylidene)-5-bromo-1H-indole-2-carbohydrazide (N-5-BIC) represents one of these chemicals exhibiting remarkable anti-angiogenesis and anti-proliferation features. The study aimed to investigate the antiangiogenic, antioxidant, and antiproliferative activities of a carbohydrazide indole derivative, N-5-BIC. The ex vivo rat aorta ring (RAR), DPPH, and chick chorioallantois membrane (CAM) assays were employed to assess the N-5-BIC antiangiogenic and antioxidant activities. The MTT assay investigated the anti-proliferative activity in the human umbilical vascular endothelial cells (HUVEC) cell line. The VEGF gene expression level in the colon cancer (HCT116) cell line was evaluated using quantitative real-time polymerase chain reaction (RT-PCR). N-5-BIC demonstrated a substantial and dose-dependent inhibition of blood vessel growth, resulting in an 87.37% reduction at a concentration of 100 μg/ml compared to the negative control (DMSO 1%) in the RAR assay. Additionally, N-5-BIC exhibited a significant decrease in DPPH free radicals in a concentration-dependent manner, with an IC50 value of 129.6 µg/ml. The in vivo CAM assay confirmed a significant regression in blood vessels compared to the negative control. Furthermore, N-5-BIC demonstrated low to non-toxic effects on the HUVEC cell line, with an IC50 value of 1681 μg/ml. The RT-PCR study revealed a significant reduction in VEGF gene expression at doses of 200 and 400 µg/ml as compared to control cells. N-5-BIC has resilient anti-angiogenic properties, which may be attributed to its extensive anti-proliferative and free radical neutralizing properties.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The combination of neurotropic B vitamins (B1, B6, and B12) is superior to individual B vitamins in promoting neurite growth in vitro.","authors":"Melissa L D Rayner, Arnaud J Ruiz, Christian Viel","doi":"10.1007/s11626-025-01024-3","DOIUrl":"10.1007/s11626-025-01024-3","url":null,"abstract":"","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"264-267"},"PeriodicalIF":1.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11978699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143556752","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}

{"title":"Adipose-derived stem cells regulate mitochondrial dynamics to alleviate the aging of HFF-1 cells.","authors":"Qi Luo, Ling Liu","doi":"10.1007/s11626-025-01017-2","DOIUrl":"10.1007/s11626-025-01017-2","url":null,"abstract":"<p><p>The objective of this study is to explore how adipose-derived stem cells (ASCs) regulate mitochondrial structure and function and the impact of this regulation on slowing cellular senescence. HFF-1 cells were induced by H₂O₂ to establish a cellular senescence model, and ASCs or Mdivi-1 (mitochondrial fission inhibitor) was added. MTT examined the cell proliferation; flow cytometry detected mitochondrial membrane potential as well as apoptosis and cell cycle; kit measured ATP production; ELISA analyzed the levels of interleukin-6 (IL-6), interleukin 1 beta (IL-1β), tumor necrosis factor alpha-like (TNF-α), glutathione (GSH), malondialdehyde (MDA), and superoxide dismutase (SOD); Western blotting and qRT-PCR detected the expression of protein and mRNA levels; and β-galactosidase staining observed the degree of cellular senescence. Compared to normal HFF-1 cells, senescent HFF-1 cells exhibited weaker proliferative capacity, marked apoptosis, and G0-G1 cell cycle arrest. These cells also showed lower mitochondrial membrane potential and ATP production, higher expression of inflammatory factors, oxidative damage, and increased levels of senescence. Treatment with Mdivi-1 or ASCs enhanced HFF-1 cell proliferation, reduced apoptosis and cell cycle arrest, increased mitochondrial membrane potential and ATP production, decreased the expression of inflammatory factors, and mitigated oxidative stress, thereby reducing the degree of cellular senescence. Concurrent intervention with Mdivi-1 and ASCs further diminishes the impacts of cellular senescence. In conclusion, ASCs regulate mitochondrial dynamics (promoting mitochondrial fusion and inhibiting mitochondrial fission), enhance ATP production, and upregulate mitochondrial membrane potential, thereby alleviating cell cycle arrest, apoptosis, inflammatory responses, and oxidative stress induced by senescence in HFF-1 cells.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"357-367"},"PeriodicalIF":1.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143052374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of IGF-1 on cartilage injury in bone marrow mesenchymal stem cells through the BMP2-Smad1/5 signaling pathway.","authors":"HuiYue Ye, Liang Shao","doi":"10.1007/s11626-025-01015-4","DOIUrl":"10.1007/s11626-025-01015-4","url":null,"abstract":"<p><p>The objective of this study is to analyze the effect of insulin-like growth factor-1 (IGF-1) in bone marrow mesenchymal stem cells (BMSCs) on cartilage injury and explore the regulatory mechanism of IGF-1 on the bone morphogenetic protein 2 (BMP2)-Smad1/5 signaling pathway. We cultivated rat BMSCs in vitro and observed their cell morphology using an inverted microscope. Flow cytometry was used to identify the surface antigen expression of BMSCs. IL-1β is used to induce rat chondrocyte ATDC5 to construct a cartilage injury model. We integrated IGF-1 overexpressed BMSCs, empty vector transfected BMSCs, and BMSCs with IL-1, respectively. IL-1β-induced ATDC5 cells were co-cultured for 24 h. We recorded them as BMSCs + IGF-1 group, BMSCs + empty vector group, BMSCs group, and normal cultured ATDC5 cells as the control group. qRT-PCR and Western blot were used to detect IGF-1 mRNA and protein levels in each group. CCK-8 experiment and flow cytometry were used to detect cell proliferation and apoptosis in each group. ELISA is used to detect the levels of TNF-α, IL-8, and IL-6. Western blot was used to detect protein levels of Bax, Bcl-2, Cleaved Caspase-3, Aggrescan, Col II, MMP-1, MMP-13, BMP2, and p-Smad1/5 in each group. Fifty rats were randomly divided into a control group, a model group, a BMSCs group, a BMSCs + empty body group, and a BMSCs + IGF-1 group using a random number table method, with 10 rats in each group. We evaluated cartilage repair using the O'Driscoll scoring system and Mankin's scoring system. HE staining was used to observe pathological changes in cartilage tissue. qRT-PCR and Western blot were used to detect the expression levels of cartilage repair-related genes OC, GSK-3β, and Runx2 in various cartilage tissues. Overexpression of IGF-1 in BMSCs could enhance IL-1β-induced ATDC5 cell survival rate and the protein level of Bcl-2; reduce apoptosis rate and the protein levels of Bax and Cleaved Caspase-3; decrease the levels of IL-6, TNF-α, and IL-8; increase the protein levels of BMP2, p-Smad1/5, Aggrescan, and Col II; and reduce the protein levels of MMP-1 and MMP-13 (P < 0.05). Compared with the model group, the O'Driscoll score in the BMSCs group, the BMSCs + empty body group, and the BMSCs + IGF-1 group was increased; Mankin's score was decreased; and the expression levels of OC, GSK-3β, and Runx2 were decreased (P < 0.05). Compared with the BMSCs group and BMSCs + empty body group, the O'Driscoll score in the BMSCs + IGF-1 group was increased, Mankin's score was decreased, and the expression levels of OC, GSK-3β, and Runx2 were decreased (P < 0.05). Overexpression of IGF-1 in BMSCs could inhibit IL-1β-induced chondrocyte apoptosis, promote cell proliferation, reduce the secretion of inflammatory factors, alleviate chondrocyte damage, and promote cartilage tissue repair. Its mechanism may be related to the activation of the BMP2-Smad1/5 signaling pathway.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"340-356"},"PeriodicalIF":1.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11978553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566678","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}