Cellular signalling最新文献

{"title":"mTOR/p70S6K signaling pathway promotes fibrillin-1 expression in AKI-to-CKD transition post CA/CPR.","authors":"Xiaohui Zhao, Limin Wang","doi":"10.1016/j.cellsig.2025.111624","DOIUrl":"https://doi.org/10.1016/j.cellsig.2025.111624","url":null,"abstract":"<p><p>The possible involvement of mTOR/p70S6K signaling in mediating Fibrillin-1 expression during the transition from acute kidney injury (AKI) to chronic kidney disease (CKD) after cardiac arrest and cardiopulmonary resuscitation (CA/CPR). A CA/CPR AKI model was established using male C57BL/6 mice aged 8-12 weeks. The expression of Fibrillin-1 and activation of the mTOR/p70S6K signaling pathway in kidney tissues were assessed at different time points. Rapamycin, administered intraperitoneally, inhibited the mTOR/p70S6K signaling pathway in CA/CPR AKI mice. Tissue immunofluorescence and immunohistochemistry were used to detect the injury, fibrosis, and inflammatory cell infiltration in renal tissues. The expression level of Fibrillin-1 and components of the mTOR/p70S6K signaling pathway, while ELISA quantified levels of inflammatory factors in renal tissues. Results showed that Fibrillin-1 expression progressively increased alongside enhanced mTOR/p70S6K signaling in the renal tissues of CA/CPR AKI mice. Inhibition of mTOR/p70S6K signaling by rapamycin reduced Fibrillin-1 expression, collagen deposition, and α-SMA levels, alleviating renal injury and decreasing macrophage and T cell infiltration, as well as inflammatory factor production. Conversely, combining rapamycin with Fibrillin-1 overexpression exacerbated renal injury and increased inflammatory factor production. Activation of the mTOR/p70S6K pathway upregulates Fibrillin-1 expression, potentially facilitating the progression from AKI to CKD in CA/CPR mice.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111624"},"PeriodicalIF":4.4,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TFEB-dependent autophagy-lysosomal pathway is required for NRF2-driven antioxidative action in obstructive sleep apnea-induced neuronal injury","authors":"Junxiu Song ,&nbsp;Tian Wang ,&nbsp;Jau-Shyong Hong ,&nbsp;Yubao Wang ,&nbsp;Jing Feng","doi":"10.1016/j.cellsig.2025.111630","DOIUrl":"10.1016/j.cellsig.2025.111630","url":null,"abstract":"<div><div>Nearly one billion individuals worldwide suffer from obstructive sleep apnea (OSA) and are potentially impacted by related neurodegeneration. TFEB is considered a master regulator of autophagy and lysosomal biogenesis, but little is known about its role in neuronal oxidative stress and resultant injury induced by OSA. This study aimed to investigate these issues. Here, we demonstrated that neuronal TFEB induction is repressed in OSA mouse models. Activation of a TFEB-dependent autophagy-lysosomal pathway (ALP) reduces hippocampal neuronal cell death and mitigates OSA-related cognitive impairment. Neuronal NRF2 induction was also found to be defective in OSA mouse models. A series of staining assays for HO1, SOD3, ROS, GSH, 8-OHdG, MDA and PI revealed that enhancement of NRF2 expression restores neuronal redox balance and protects hippocampal neurons. We then identified a novel interplay between TFEB-dependent ALP and NRF2-mediated relief of oxidative stress. Inhibition of NRF2 hinders TFEB expression and lysosomal biogenesis. Conversely, knockdown of TFEB or blocking autophagy dampens the antioxidative effect of NRF2. Our findings highlight the unexpected and crucial role of TFEB-dependent ALP as a downstream event of NRF2 in NRF2-promoted redox balance. This study provides novel insights into the mechanism behind NRF2-driven antioxidative action and the regulation of TFEB-dependent ALP.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"128 ","pages":"Article 111630"},"PeriodicalIF":4.4,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058329","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}

{"title":"Alternative splicing of vascular calcification: Insights, opportunities, and challenges","authors":"Yingkun Sheng ,&nbsp;Hewen Wei ,&nbsp;Shengmin Lu ,&nbsp;Weiling Hong","doi":"10.1016/j.cellsig.2025.111626","DOIUrl":"10.1016/j.cellsig.2025.111626","url":null,"abstract":"<div><div>Vascular calcification(VC) significantly increases the risk of cardiovascular events, leading to thickening of the myocardium and arteries, coronary heart disease, heart failure, and potentially triggering myocardial infarction and sudden cardiac death. Although VC is a reversible process, there are currently no methods or medications in clinical practice that can completely reverse or cure it. The current treatment strategies primarily focus on slowing the progression of VC and exploring new diagnostic and therapeutic approaches, making the identification of early diagnostic markers for VC particularly important. Alternative splicing(<em>AS</em>)has extensive potential in clinical applications as a biomarker, including in disease diagnosis and therapeutic targeting. This article provides an overview of the roles played by different isoforms of biomarkers in VC, with the aim of offering insights for early diagnosis and disease monitoring of VC.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111626"},"PeriodicalIF":4.4,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"m6A modified ATG9A is required in regulating autophagy to promote HSCs activation and liver fibrosis","authors":"Tingjuan Huang ,&nbsp;Ziyi Shang ,&nbsp;Lina Nie ,&nbsp;Haichao Diao ,&nbsp;Qizhi Shuai ,&nbsp;Junjie Ren ,&nbsp;Jun Xu ,&nbsp;Jun Xie","doi":"10.1016/j.cellsig.2025.111619","DOIUrl":"10.1016/j.cellsig.2025.111619","url":null,"abstract":"<div><div>Hepatic stellate cells (HSCs) are the central link of the occurrence and development of hepatic fibrosis, and autophagy promotes HSCs activation. N6-methyladenosine (m6A) RNA modification can also control autophagy by targeting selected autophagy-associated genes. but up to now, little research has been done on the m6A modification autophagy-related genes (ATGs) in hepatic fibrosis. Here, we identify ATG9A as a previously unrecognized m6A modified ATG using m6A-sequencing (m6A-seq). Importantly, ATG9A is upregulated in liver fibrosis mice and primary biliary cirrhosis (PBC) patient liver tissue. Mechanistically, based on the presence of m6A binding sites on ATG9A, ATG9A promotes HSCs autophagy in an m6A dependent manner, thereby enhancing HSCs activation. Noteworthy, FTO is identified as the upstream of ATG9A, and knockdown of ATG9A can prevent FTO-induced HSCs autophagy and activation. In bile duct ligation (BDL) or CCL4-induced liver fibrosis mouse models, lowering ATG9A alleviated liver fibrosis through PI3K/AKT/mTOR pathway and TGFβ1/smad3 pathway. Taken together, our results provided that ATG9A is a potential prognostic biomarker and therapeutic target for patients with liver fibrosis.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111619"},"PeriodicalIF":4.4,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A multi-omics analysis reveals KDELR1 promotes malignant progression and correlates with tumor microenvironment in head and neck squamous cell carcinoma","authors":"Wenjin Wang ,&nbsp;Bokai Yun ,&nbsp;Zhuqin Xiang ,&nbsp;Xiaoyong Liu ,&nbsp;Chen Yi ,&nbsp;Shengqi Ouyang ,&nbsp;Xiliu Zhang ,&nbsp;Gan Xiong ,&nbsp;Zehang Zhuang ,&nbsp;Cheng Wang","doi":"10.1016/j.cellsig.2025.111613","DOIUrl":"10.1016/j.cellsig.2025.111613","url":null,"abstract":"<div><div>KDELR1, a constituent of the KDEL endoplasmic reticulum protein retention receptors family, is implicated in immune responses and cancers progression. In this study, we delineate the clinicopathological significance and oncogenic role of KDELR1 in head and neck squamous cell carcinoma (HNSCC) through a comprehensive multi-omics approach. KDELR1 expression is correlated with tumor grade, tumor stage, lymph node metastasis, clinical stage and poor prognosis in HNSCC. Moreover, our results indicate a marked upregulation of KDELR1 expression in primary tumor tissues compared to normal and dysplasia tissues. Furthermore, increased KDELR1 expression is associated with tumor progression and indicates an unfavorable prognosis in HNSCC. Functional enrichment analysis highlights the involvement of KDELR1 in HNSCC malignant progression. Depletion of KDELR1 inhibits proliferation, stemness, migration and invasion in HNSCC cells. Bioinformatics analysis results indicate that KDELR1 promotes HNSCC progression with regulating wnt signaling pathway and CTNNB1 expression. Of note, KDELR1 is associated with HNSCC tumor microenvironment compositions, especially positively correlating with cancer associated fibroblasts and negatively correlating with CD8+ T cells and B cells infiltration. Collectively, these findings indicate that KDELR1 as an oncogene in driving progression and correlates with tumor microenvironment, suggesting its potential as a promising biomarker and a therapeutic target in HNSCC.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111613"},"PeriodicalIF":4.4,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058277","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}

{"title":"Free fatty acids derived from lipophagy enhanced resistance to anoikis by activating Src in high-invasive clear cell renal cell carcinoma cells","authors":"Mengmeng Wu ,&nbsp;Guijuan Chen ,&nbsp;Xin Li ,&nbsp;Wenliang Ma ,&nbsp;Yi Chen ,&nbsp;Yi Gong ,&nbsp;Hao Zheng ,&nbsp;Gongming Gu ,&nbsp;Yibing Ding ,&nbsp;Ping Dong ,&nbsp;Weidong Ding ,&nbsp;Luqing Zhang ,&nbsp;Weidong Gan ,&nbsp;Dongmei Li","doi":"10.1016/j.cellsig.2025.111622","DOIUrl":"10.1016/j.cellsig.2025.111622","url":null,"abstract":"<div><div>Autophagy-mediated anoikis resistance plays a critical role in the initiation of tumor metastasis. Therefore, we investigated the role and mechanism of anoikis resistance mediated by free fatty acids (FFAs) derived from lipophagy in highly invasive clear cell renal cell carcinoma (ccRCC). Here, we found that the highly invasive ccRCC cell line Himi exhibited enhanced resistance to anoikis and elevated lipophagy levels. The increased lipophagy observed in Himi ccRCC cells contributed to their resistance to anoikis. The nonreceptor tyrosine kinase Src was significantly upregulated in Himi cells cultured under suspension conditions and in patients with poor prognoses. The underlying mechanism revealed that the FFAs released from lipophagy activated the phosphorylated Tyr419 site of Src, thereby promoting ccRCC invasion, facilitating epithelial–mesenchymal transition (EMT), enhancing angiogenesis, and conferring resistance to anoikis. Therefore, the present study revealed that FFAs generated from the degradation of lipid droplets <em>via</em> lipophagy enhanced resistance to anoikis by activating the phosphorylated Tyr419 site of Src in highly invasive ccRCC.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111622"},"PeriodicalIF":4.4,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HDAC2 promotes colorectal tumorigenesis by triggering dysregulation of lipid metabolism through YAP1.","authors":"Zhanghan Chen, Weifeng Hong, Bing Li, Dongli He, Zhong Ren, Mingyan Cai, Yirong Cheng, Jingyi Liu, Enpan Xu, Yanyun Du, Yuelun Dong, Shilun Cai, Qiang Shi, Zhipeng Qi, Yunshi Zhong","doi":"10.1016/j.cellsig.2025.111627","DOIUrl":"https://doi.org/10.1016/j.cellsig.2025.111627","url":null,"abstract":"<p><p>Dysfunction of lipid metabolism is important for the development and progression of colorectal cancer, but the underlying mechanisms remain unclear. Here, HDAC2 was identified as highly expressed in both adenoma and colorectal cancer. We aimed to explore the roles and mechanisms of HDAC2 in lipid metabolism in colorectal cancer. HDAC2 expression in adenoma and colorectal cancer tissues was measured using tissue arrays. The function of HDAC2/YAP1 was identified using in vitro and in vivo experiments. Coimmunoprecipitation experiments, DNA pull-down assays, luciferase analyses, and ChIP-qPCR (Chromatin Immunoprecipitation-quantitative real-time polymerase chain reaction) assays were used to identify the potential mechanisms of HDAC2. We found that HDAC2 can disrupt lipid metabolism in colorectal cancer by mediating the deacetylation of YAP1. Mechanistically, HDAC2 can bind to YAP1 and mediate deacetylation of the K280 site of YAP1. Furthermore, the deacetylation of YAP1 reduces the efficiency of its binding to the ZMYND11 promoter region, exacerbating lipid metabolism disorders, which in turn reduce lipid accumulation and increase lipid catabolism in colorectal cancer cells. Our study identified a novel regulatory mechanism of lipid metabolism in colorectal cancer in which HDAC2 increases lipid catabolism by regulating the deacetylation of the K280 site of YAP1, revealing that HDAC2 promotes tumor progression through the regulation of lipid metabolism.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111627"},"PeriodicalIF":4.4,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zn2+ protects H9C2 cardiomyocytes by alleviating MAMs-associated apoptosis and calcium signaling dysregulation","authors":"Jiabao Guo ,&nbsp;Tingting Ma ,&nbsp;Bingyu Wang ,&nbsp;Bohan Xing ,&nbsp;Luyao Huang ,&nbsp;Xiaoyi Li ,&nbsp;Huan Zheng ,&nbsp;Yonggui He ,&nbsp;Jinkun Xi","doi":"10.1016/j.cellsig.2025.111629","DOIUrl":"10.1016/j.cellsig.2025.111629","url":null,"abstract":"<div><h3>Purpose</h3><div>This study aims to investigate whether zinc ion (Zn²⁺) alleviates myocardial ischemia-reperfusion injury (MIRI) through the MAM-associated signaling pathway and to explore its impact on ERS and calcium overload.</div></div><div><h3>Methods</h3><div>H9C2 cells were cultured in a DMEM supplemented with 10 % fetal bovine serum and 1 % antibiotic solution. A MIRI model was established through simulated ischemia and reoxygenation with Zn²⁺ treatment in a complete medium. Cells were then treated with the MCU inhibitor ruthenium red (RR), the MCU activator spermine (SP), and siRNAs targeting Bap31, MCU, VDAC1, and FUNDC1. Cell viability was assessed using MTT and CCK-8 assays. Lactate dehydrogenase (LDH) levels were measured with a commercial kit. Western blot was performed to detect protein expression levels. Cell apoptosis, intracellular zinc, calcium levels, mitochondrial membrane potential, and protein fluorescence changes were observed using laser scanning confocal microscopy.</div></div><div><h3>Results</h3><div>Compared to the control group, cell viability was significantly reduced in the I/R group, accompanied by increased expression of apoptosis and calcium overload-related proteins increased cell injury, apoptosis, calcium overload, and a decrease in mitochondrial membrane potential. Zn²⁺ treatment reversed the detrimental effects of I/R in the I/R + Zn²⁺ group. When Bap31, VDAC1, FUNDC1, or MCU were silenced using siRNA, the protective effect of Zn²⁺ was further enhanced (<em>P</em> &lt; 0.05).</div></div><div><h3>Conclusions</h3><div>Ischemia-reperfusion (I/R) leads to cardiomyocyte injury and apoptosis. Zn²⁺ downregulates the expression of key apoptotic proteins through the Bap31/Fis1 pathway and regulates MCU activity through the IP3R1-GRP75-VDAC1 and IP3R2/FUNDC1 pathways to alleviate calcium overload and ultimately protect cardiomyocytes after I/R.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111629"},"PeriodicalIF":4.4,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA SNHG5 induces CAFs-like phenotype and autophagy of AML-MSCs via PTBP1/ATG5 axis to confer chemoresistance of AML cells.","authors":"Yuan Song, Lili Hu, Jing Cheng, Zhenjiang Li, Jifu Zheng","doi":"10.1016/j.cellsig.2025.111625","DOIUrl":"https://doi.org/10.1016/j.cellsig.2025.111625","url":null,"abstract":"<p><strong>Background: </strong>Acute myeloid leukemia (AML) is still a threaten to human health due to its high occurrence and poor prognosis. Mesenchymal stem cells (MSCs) in bone marrow microenvironment (BMM) play a critical role in the development of AML. This study elucidated the interaction between MSCs and AML cells and its underlying mechanism.</p><p><strong>Method: </strong>MSCs were isolated, identified, and co-cultured with AML cells. qRT-PCR, Western blotting and immunofluorescence were used to determine molecule expression. Cell viability and apoptosis were determined by CCK-8 and flow cytometry. Exosomes were isolated and characterized, and PKH26 was used for monitoring exosome internalization. RNA-FISH was used to determine the localization of SNHG5. RIP, RNA-pull down and ChIP assays were used to evaluate the molecular interaction.</p><p><strong>Results: </strong>SNHG5 expression was up-regulated and positively correlated with cancer-associated fibroblasts (CAFs)-related biomarkers in MSCs. AML cells-derived exosomes delivered SNHG5 to enhance its expression in MSCs. SNHG5 overexpression induced CAFs-like phenotype and autophagy in MSCs that led to daunorubicin resistance of AML cells. Mechanistically, SNHG5 stabilized autophagy related 5 (ATG5) mRNA by interaction with polypyrimidine tract-binding protein 1 (PTBP1).</p><p><strong>Conclusion: </strong>AML cells-derived exosomal lncRNA SNHG5 triggered CAFs-like phenotype and autophagy of AML-MSCs via interaction with PTBP1 to increase ATG5 mRNA stability, thereby leading to chemoresistance of AML cells.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111625"},"PeriodicalIF":4.4,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ANXA2 promotes chondrocyte differentiation and fracture healing by regulating the phosphorylation of STAT3 and PI3K/AKT signaling pathways","authors":"Xinru Wang,&nbsp;Wei Dong,&nbsp;Xinyi Wang,&nbsp;Jiawei Wang","doi":"10.1016/j.cellsig.2025.111617","DOIUrl":"10.1016/j.cellsig.2025.111617","url":null,"abstract":"<div><div>Fractures are common and serious skeletal injuries, and accelerating their healing while alleviating patient suffering remains a clinical challenge. Annexin A2 (ANXA2) is a widely distributed, calcium-dependent, phospholipid-binding protein involved in bone remodeling. However, its role in chondrocyte differentiation and endochondral ossification remains unclear. In this study, we found that ANXA2 is expressed in chondrocytes during growth plate development and fracture healing, as well as during chondrocyte differentiation and maturation <em>in vitro</em>, with its highest expression occurring in the most active differentiation phase. Moreover, ANXA2 knockdown inhibited chondrocyte differentiation, while its overexpression significantly promoted it. We also demonstrated that ANXA2 regulates the chondrogenic and hypertrophic differentiation by mediating the phosphorylation and nuclear translocation of STAT3, as well as activating the PI3K/AKT pathway. Finally, recombinant ANXA2 protein was injected into the tibial fracture sites of mice, verifying its role in promoting endochondral ossification during fracture healing. In conclusion, our study shows that ANXA2 promotes chondrocyte differentiation, partially through the STAT3 and PI3K/AKT pathways. These findings provide insights that could aid in developing new therapies to enhance fracture healing.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111617"},"PeriodicalIF":4.4,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}