Cellular signalling最新文献

{"title":"ZFP36 reverses chemoresistance by disrupting lipid droplets accumulation in non-small cell lung cancer","authors":"Zhe Wang ,&nbsp;Peng Hou ,&nbsp;Yang Wu ,&nbsp;Jiaojiao Dai ,&nbsp;Ping Zhao ,&nbsp;Xiaoxun Cheng ,&nbsp;Zhengze Hu ,&nbsp;Lingling Zhang ,&nbsp;Jinghan Hua","doi":"10.1016/j.cellsig.2025.112119","DOIUrl":"10.1016/j.cellsig.2025.112119","url":null,"abstract":"<div><div>Acquired chemoresistance is a major factor contributing to non-small cell lung cancer (NSCLC) therapy failure, and there is no effective intervention target. Recent evidence suggests that disrupting the altered lipid metabolism could sensitize cancer cells to chemotherapy treatments. Here, we demonstrate that zinc finger protein 36 (ZFP36) downregulation promotes the accumulation of lipid droplets (LDs) through the ZFP36-mediated fatty acid synthase (FASN) mRNA decay process, contributing to NSCLC progression and the acquisition of chemoresistance. We advocate that enhancing the suppressive role of ZFP36 on LDs accumulation to treat chemoresistant NSCLC, based on its novel regulatory mechanism in chemoresistance.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"136 ","pages":"Article 112119"},"PeriodicalIF":3.7,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145060392","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":"The effects of UCN2 on neural cell function of spinal cord injury rats facilitate post-injury neuronal regeneration","authors":"Yin-Jie Hu ,&nbsp;Peng Liu ,&nbsp;Xiao-Long Tang ,&nbsp;Bing-Rong Li ,&nbsp;Long Yuan ,&nbsp;Fang-Fang Dou ,&nbsp;Ling Zhao ,&nbsp;Bi-Meng Zhang","doi":"10.1016/j.cellsig.2025.112134","DOIUrl":"10.1016/j.cellsig.2025.112134","url":null,"abstract":"<div><div>Spinal cord injury (SCI) is a devastating condition with high disability rates and lacks effective treatments. This study investigated the therapeutic potential of Urocortin 2 (UCN2) for promoting neurofunctional recovery. In a rat model of T10 spinal cord transection, daily intraperitoneal UCN2 treatment, initiated two days post-injury, significantly improved hindlimb motor function by day 14. We found that the UCN2 receptor, CRHR2, is expressed in neurons, astrocytes, and microglia. In vivo, UCN2 administration reduced neuronal apoptosis and neurofilament damage, suppressed microglial activation, and promoted the conversion of neurotoxic A1 astrocytes to a regenerative A2 phenotype. These beneficial effects were mediated by the activation of the cAMP-PKA signaling pathway, evidenced by the upregulation of PKA, CREB, and Bcl-2, and downregulation of NF-κB, RhoA, and Bax. Complementary in vitro experiments confirmed that UCN2 directly promotes axonal regeneration, inhibits neuronal apoptosis, enhances the secretion of GDNF from astrocytes, and suppresses the inflammatory NF-κB pathway in microglia. In conclusion, UCN2 facilitates axonal regeneration and functional recovery in SCI by activating the cAMP-PKA pathway, which in turn modulates neuronal survival, glial phenotype, and neuroinflammation, highlighting its significant therapeutic potential.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"136 ","pages":"Article 112134"},"PeriodicalIF":3.7,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063613","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":"GPR108 deficiency promotes urate-induced renal interstitial fibrosis","authors":"Deping Xu ,&nbsp;Ping Yang ,&nbsp;Wei Song ,&nbsp;Kainan Liao ,&nbsp;Dandan Zang ,&nbsp;Qiang Zhou ,&nbsp;Haisheng Zhou","doi":"10.1016/j.cellsig.2025.112129","DOIUrl":"10.1016/j.cellsig.2025.112129","url":null,"abstract":"<div><div>Uric acid, a product of purine metabolism, is predominantly excreted via the kidneys. Chronic hyperuricemia, often driven by high-purine diets, contributes to renal injury marked by inflammation, tubular damage, and interstitial fibrosis with epithelial-mesenchymal transition (EMT). G protein-coupled receptor 108 (GPR108), a negative regulator of NF-κB-mediated inflammation, remains unexplored in hyperuricemia-induced chronic kidney disease (CKD). This study investigates GPR108's role in uric acid nephropathy using adenine-fed mice and in vitro models. <em>Gpr108</em>-deficient mice exhibited aggravated renal fibrosis, EMT activation, and elevated cytokine levels compared to controls. In vitro, renal tubular epithelial cells of primary cultured <em>Gpr108</em> knockout mice heightened sensitivity to uric acid-induced EMT, accompanied by increased TGF-β1 production and NF-κB activation. These findings demonstrate that GPR108 deficiency exacerbates renal inflammation and fibrosis by amplifying NF-κB-driven EMT and TGF-β1 signaling. Our study identifies GPR108 as a protective modulator in hyperuricemia-induced CKD, highlighting its potential as a therapeutic target to mitigate renal interstitial fibrosis.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"136 ","pages":"Article 112129"},"PeriodicalIF":3.7,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063589","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":"Identification of the PP1 interactome in human dental pulp: Insights for regenerative strategies","authors":"Anna Kobrock ,&nbsp;Daniela Patrício ,&nbsp;Bárbara Matos ,&nbsp;Eduardo Zarzuela ,&nbsp;Javier Muñoz ,&nbsp;John Howl ,&nbsp;Pedro S. Gomes ,&nbsp;Margarida Fardilha","doi":"10.1016/j.cellsig.2025.112132","DOIUrl":"10.1016/j.cellsig.2025.112132","url":null,"abstract":"<div><h3>Background</h3><div>Dental caries are one of the most prevalent chronic diseases worldwide affecting all age groups. Current therapeutic strategies are technically demanding and invasive procedures that only address the restoration of dental pulp. Upon damage, mineralized tissues and dental pulp are affected, activating signalling cascades that promote their repair and regeneration through stem cells differentiation into odontoblasts-like cells. Protein phosphatase 1 (PP1) participates in a panoply of cellular events, including those related with regenerative outcomes, such as odontogenic differentiation, highlighting the potential of its modulation.</div></div><div><h3>Methods</h3><div>Here we evaluated the expression of PP1 isoforms in dental pulp cells lines. We also characterized the PP1 interactome in dental pulp and identified potential interactors involved in repair and regenerative processes.</div></div><div><h3>Results</h3><div>The expression of all PP1 isoforms (α, β and γ) was detected in human dental cell lines. Moreover, a total of 258 proteins were identified as PP1γ regulatory interactors of protein phosphatase 1 (RIPPOs) in dental pulp, through a combination of a bioinformatic and co-immunoprecipitation/mass spectrometry analyses. Among these proteins, RRBP1 and THBS1 are promising targets, due to their roles in modulation of the regenerative response and in odontoblasts differentiation and mineralization.</div></div><div><h3>Conclusion</h3><div>This is the first reported PP1 interactome in dental pulp that identifies potential targets to modulate PP1 activity and potentially promote dental pulp regeneration.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"136 ","pages":"Article 112132"},"PeriodicalIF":3.7,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063602","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":"Hispolon reduces mitochondrial dysfunction and improves fibrosis of diabetes nephropathy by activating AMPK signal and inhibiting mPTP opening","authors":"Yapeng Wang ,&nbsp;Ajau Danis ,&nbsp;Xueyi Wang ,&nbsp;Jia Ren ,&nbsp;Teng Ma ,&nbsp;Ruixiao Wang","doi":"10.1016/j.cellsig.2025.112130","DOIUrl":"10.1016/j.cellsig.2025.112130","url":null,"abstract":"<div><div>Diabetic nephropathy progression is linked to the AMPK/SIRT1/PGC-1α signaling pathway. Hispolon's potential in improving mitochondrial function and treating diabetic nephropathy via this pathway was unclear. This study used db/db mice and high glucose-induced SV40 MES 13 cells to explore Hispolon's renoprotective mechanisms.</div><div>In vivo, db/db mice showed glomerular damage, collagen deposition, glycoprotein accumulation, and elevated serum creatinine and urea nitrogen. Hispolon intervention improved these features and parameters. It reduced renal MDA levels, enhanced SOD activity, suppressed pro-inflammatory mediators, and downregulated fibrosis markers. Western blot analysis showed Hispolon restored p-AMPK, SIRT1, and PGC-1α protein levels. In vitro, Hispolon enhanced cell viability, inhibited apoptosis, and reversed high glucose-induced oxidative stress and inflammation in SV40 MES 13 cells. It improved mitochondrial energy metabolism by restoring mitochondrial membrane potential, increasing ATP production, and inhibiting abnormal mPTP opening. Mechanistic studies confirmed that the AMPK/SIRT1/PGC-1α signaling cascade is key for Hispolon's regulation of mPTP dynamics. In conclusion, Hispolon slows diabetic nephropathy progression by activating the AMPK/SIRT1/PGC-1α pathway, inhibiting mPTP opening, and improving mitochondrial dysfunction.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"136 ","pages":"Article 112130"},"PeriodicalIF":3.7,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058302","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":"Targeting ferroptosis in cervical cancer: Mechanistic insights and therapeutic opportunities","authors":"Shunji An ,&nbsp;Anna Han ,&nbsp;Zhenhua Lin ,&nbsp;Haiyan Quan","doi":"10.1016/j.cellsig.2025.112122","DOIUrl":"10.1016/j.cellsig.2025.112122","url":null,"abstract":"<div><div>Cervical cancer is the fourth most common malignancy among women worldwide. Despite standard chemoradiotherapy, a significant number of patients experience recurrence or distant metastasis. Accumulating evidence highlights ferroptosis—an iron-dependent form of regulated cell death driven by lipid peroxidation (LPO)—as a key mechanism influencing cervical carcinogenesis and treatment outcomes. Ferroptosis is marked by intracellular iron overload, excessive reactive oxygen species (ROS) production, and loss of redox balance. This review provides a comprehensive overview of the emerging roles of ferroptosis in the initiation, progression, and therapeutic resistance of cervical cancer. We outline the regulatory networks and signaling pathways that control ferroptosis in cervical cancer cells and assess the therapeutic potential of inducing ferroptosis using small-molecule compounds and nanomedicine approaches. Additionally, we discuss the prognostic value of ferroptosis-related genes (FRGs), their association with immune infiltration, and their implications for personalized immunotherapy. Collectively, these insights emphasize the translational promise of targeting ferroptosis as a novel strategy for precision oncology and targeted therapy in cervical cancer.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"136 ","pages":"Article 112122"},"PeriodicalIF":3.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145045753","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":"Tenvermectin B, a novel macrocyclic lactone antibiotic, suppresses glioblastoma progression by targeting RhoJ","authors":"Chenyi Nie ,&nbsp;Hongsheng Liang ,&nbsp;Jiaxin Zhou ,&nbsp;Hefei Liu ,&nbsp;Ruiqiang Shang ,&nbsp;Hongge Yang ,&nbsp;Wang Jiang ,&nbsp;Huan Qi ,&nbsp;Jidong Wang ,&nbsp;Aili Gao","doi":"10.1016/j.cellsig.2025.112117","DOIUrl":"10.1016/j.cellsig.2025.112117","url":null,"abstract":"<div><h3>Background</h3><div>The migratory and invasive behavior of glioblastoma (GBM) poses significant challenges for treatment, and the underlying mechanisms require further exploration. While macrolide antibiotics exhibit antitumor activity, the antitumor effects and molecular mechanisms of the novel macrolide TVM B remain unclear. This study aimed to investigate its efficacy against GBM and elucidate the mechanisms by which it modulates GBM cell migration and invasion.</div></div><div><h3>Methods</h3><div>First, the cytotoxicity of TVM B was evaluated using the MTT assay. In vivo, a xenograft mouse model was established, and the drug was administered via intraperitoneal injection. Western blot and pathological staining were performed to investigate the effects of TVM B on tumor growth. Used RNA-seq data to explore its potential mechanism of action, and performed molecular docking to identify potential targets. In vitro validation experiments included the wound healing assay, Transwell migration and invasion assays, Tube formation Assay, RT-qPCR, Western blot, flow cytometry for apoptosis detection, and immunofluorescence staining.</div></div><div><h3>Results</h3><div>In vitro, TVM B inhibited GBM cells proliferation, induced apoptosis, and suppressed migration and invasion. TVM B abrogated the angiogenic capacity of HUVECs. In vivo xenograft experiments showed that TVM B treatment reduced Ki67 positivity, decreased the expression of MMP9, MMP2, and p-FAK in tumor tissues, and HE staining of various organs revealed no obvious toxicity. Mechanistic studies showed TVM B regulated RhoJ to inhibit cytoskeletal dynamics and FAK/Src signaling, thereby suppressing cell migration and invasion via focal adhesion modulation.</div></div><div><h3>Conclusion</h3><div>This study for the first time demonstrates that TVM B regulates cytoskeletal homeostasis via RhoJ, inhibits cell proliferation, and affects the FAK/Src pathway to ultimately suppress migration and invasion of GBM cells.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"136 ","pages":"Article 112117"},"PeriodicalIF":3.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145045754","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":"GPR91 mediates low shear stress-induced endothelial ferroptosis via EGR1-dependent GPX4 repression","authors":"Ming Su ,&nbsp;Qian Wu ,&nbsp;Yile Zhang ,&nbsp;Die Wang ,&nbsp;Chuchu Yuan ,&nbsp;Siyu Lu ,&nbsp;Lijun Liang ,&nbsp;Bo Yu ,&nbsp;Dangheng Wei","doi":"10.1016/j.cellsig.2025.112127","DOIUrl":"10.1016/j.cellsig.2025.112127","url":null,"abstract":"<div><div>Emerging evidence suggests that low shear stress (LSS) contributes to endothelial injury in atherosclerosis, yet the underlying molecular mechanisms remain incompletely understood. Here, we demonstrate that LSS triggers ferroptosis in vascular endothelial cells through a novel GPR91/EGR1/GPX4 signaling axis. By integrating bioinformatics, single-cell RNA sequencing (scRNA-seq), and ChIP-qPCR, we identified a significant correlation between LSS-responsive genes and ferroptosis-related pathways in atherosclerotic plaques. Using parallel-plate flow chamber system, we confirmed that LSS (3 dyne/cm²) induces characteristic ferroptosis markers in human vascular endothelial cells. Mechanistically, LSS upregulated GPR91, enhancing cellular mechanosensitivity, as further validated in HEK293T cells. Pharmacological inhibition of GPR91 attenuated LSS-induced ferroptosis, while its agonists exacerbated ferroptosis. RNA-seq and ChIP-qPCR identified EGR1 as a downstream of GPR91 effector that binds directly to the GPX4 promoter (M2 motif), repressing its transcription under LSS. Our findings establish GPR91 as a mechanosensitive receptor that links LSS to ferroptosis signaling via EGR1- mediated GPX4 repression, providing new therapeutic targets for shear stress-related vascular pathologies.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"136 ","pages":"Article 112127"},"PeriodicalIF":3.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145045755","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":"SHLP2 alleviates allergic asthma by inhibiting ETV5/GSDMD signaling pathway-mediated pyroptosis","authors":"Wenlong Zhang ,&nbsp;Yan Wang ,&nbsp;Chenhui Ma ,&nbsp;Shengpeng Li ,&nbsp;Yanli Zhang ,&nbsp;Xinhua Wang ,&nbsp;Shuguang Han","doi":"10.1016/j.cellsig.2025.112126","DOIUrl":"10.1016/j.cellsig.2025.112126","url":null,"abstract":"<div><h3>Background</h3><div>Allergic asthma (AA) is a lung disease characterized by impaired respiratory function and significant infiltration of inflammatory cells. Human Protein-Mimicking Peptide-2 (SHLP2) is a recently discovered mitochondria-encoded peptide that plays a crucial role in mitochondrial retrograde signaling pathways. However, its potential utility in mitigating AA remains unexplored. Our study investigates the therapeutic potential of SHLP2 in AA.</div></div><div><h3>Results</h3><div>We found that SHLP2 expression was significantly lower in the serum of patients with AA and correlated with key AA biomarkers. Exogenous SHLP2 supplementation alleviated house dust mites (HDM)-induced lung inflammation and airway barrier damage in mice. Additionally, SHLP2 ameliorated mitochondrial damage and inhibited pyroptosis in bronchial epithelial cells. At the mechanistic level, we identified a binding site between SHLP2 and the promoter region of the ETS Variant Transcription Factor 5 (ETV5) using a luciferase reporter assay. SHLP2 inhibited the transcription of downstream GSDMD, thereby suppressing pyroptosis.</div></div><div><h3>Conclusions</h3><div>Overexpression of ETV5 improved mitochondrial function and reduced pyroptosis in bronchial epithelial cells. However, exogenous SHLP2 supplementation failed to reverse the exacerbation of HDM-induced lung inflammation and airway barrier damage caused by ETV5 knockout in mice. These findings highlight SHLP2 as a key ETV5/GSDMD signaling pathway regulator, inhibiting pyroptosis and mitigating AA progression.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"136 ","pages":"Article 112126"},"PeriodicalIF":3.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039320","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":"BCAR3 confers resistance to cisplatin in head and neck squamous cell carcinoma by sustaining TGF-β/SMAD signaling","authors":"Yaning Wang ,&nbsp;Zhenyu Cheng ,&nbsp;Rui Qiao ,&nbsp;Yixuan Zhao ,&nbsp;Hui Li ,&nbsp;Hongyu Zhao ,&nbsp;Qingguo Lai ,&nbsp;Teng Xu","doi":"10.1016/j.cellsig.2025.112124","DOIUrl":"10.1016/j.cellsig.2025.112124","url":null,"abstract":"<div><div>Cisplatin-based chemotherapy serves as a first-line therapy in advanced/metastatic head and neck squamous cell carcinoma (HNSCC). However, multiple factors confer treatment resistance, severely compromising its clinical efficacy. The purpose of this study was to determine the potential driving factors underlying this resistance and to develop a reliable combination treatment agent to overcome it. Using transcriptome analysis and clinical cohorts, breast cancer anti-estrogen resistance 3 (BCAR3) was identified as a candidate gene related to the development of intrinsic cisplatin resistance in HNSCC and was verified both in vitro and in vivo. Gene set enrichment analysis revealed that TGF-β/SMAD signaling was strongly activated in BCAR3-upregulated tumors. Western blotting and flow cytometry indicated that BCAR3 increased the phosphorylation of SMAD2 and facilitated the transcriptional activation of SMAD4, which suppressed mitochondria-derived apoptosis. Moreover, inhibition of TGF-β/SMAD signaling through treatment with galunisertib achieved synergistic efficacy with cisplatin. The above findings demonstrate that BCAR3 is a positive regulator of TGF-β/SMAD signaling-mediated intrinsic cisplatin resistance. Targeting the BCAR3/TGF-β/SMAD axis might be a promising therapeutic strategy for overcoming cisplatin resistance in HNSCC.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"136 ","pages":"Article 112124"},"PeriodicalIF":3.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039228","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}