Journal of Cell Communication and Signaling最新文献_第3页

Beyond the tumor: Enhancing pancreatic cancer therapy through glutamine metabolism and innovative drug delivery 超越肿瘤：通过谷氨酰胺代谢和创新药物输送增强胰腺癌治疗

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-07-09 DOI: 10.1002/ccs3.70033

Min Su, Huan Qin, Jie Shen, Hao An, Yu Cao

{"title":"Beyond the tumor: Enhancing pancreatic cancer therapy through glutamine metabolism and innovative drug delivery","authors":"Min Su, Huan Qin, Jie Shen, Hao An, Yu Cao","doi":"10.1002/ccs3.70033","DOIUrl":"https://doi.org/10.1002/ccs3.70033","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) depends a lot on how it uses glutamine to grow quickly and stay alive. Oncogenic drivers such as KRAS, c-Myc, and HIF-1α increase how much glutamine gets taken up and broken down. Meanwhile, the bacteria in the gut and tumor itself also affect how much glutamine is available throughout the body and near the tumor. This impacts both how the tumor grows and how the immune system can detect and respond to it. Multiple strategies have emerged to disrupt this dependence: glutamine antagonists (DON and its prodrugs DRP-104, JHU-083), small-molecule glutaminase inhibitors (CB-839), antibody–drug conjugates targeting the ASCT2 transporter, and combination regimens pairing glutamine blockade with immune checkpoint inhibitors. Nanoparticle formulations—including pH-sensitive and PEGylated liposomes co-delivering DON and gemcitabine—enable targeted delivery and reduce off-target toxicity. Single-agent treatments do not work so well because the cells can adapt. They boost enzymes such as asparagine synthetase and increase how they burn fatty acids to make up for the lack of glutamine. To overcome these escape routes, future interventions must concurrently target compensatory pathways and integrate biomarker-driven patient selection. Combining glutamine-targeted agents with inhibitors of asparagine synthesis or lipid oxidation, guided by multi-omics profiling, promises a more durable therapeutic benefit and lays the groundwork for personalized treatment of PDAC.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144589549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Sirtuin 2 regulates NOD-like receptor protein 3/nuclear factor kappa B axis to promote cartilage repair in osteoarthritis Sirtuin 2调节nod样受体蛋白3/核因子κ B轴促进骨关节炎软骨修复

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-07-03 DOI: 10.1002/ccs3.70031

Xiaotian Chen, Yining Song, Fan Zhang, Fangyan Hu, Zhenfei Ding, Jianzhong Guan

{"title":"Sirtuin 2 regulates NOD-like receptor protein 3/nuclear factor kappa B axis to promote cartilage repair in osteoarthritis","authors":"Xiaotian Chen, Yining Song, Fan Zhang, Fangyan Hu, Zhenfei Ding, Jianzhong Guan","doi":"10.1002/ccs3.70031","DOIUrl":"https://doi.org/10.1002/ccs3.70031","url":null,"abstract":"Osteoarthritis (OA) is a prevalent degenerative joint disease driven by inflammation and cartilage degradation. The NOD-like receptor protein 3 (NLRP3) inflammasome and nuclear factor kappa B (NF-κB) pathway are central to OA-associated inflammation. Sirtuin 2 (SIRT2), an NAD+-dependent deacetylase, regulates inflammation and oxidative stress but its role in OA is not fully understood. This study aims to elucidate how SIRT2 modulates the NLRP3/NF-κB signaling axis to promote cartilage repair in OA. In vivo and in vitro experiments were conducted using OA mouse models and chondrocyte cultures. Single-cell RNA sequencing was performed to identify differentially expressed genes, followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. SIRT2's impact on NLRP3 and NF-κB was assessed using Western blotting (WB), real-time PCR, co-immunoprecipitation (Co-IP), and chromatin immunoprecipitation (ChIP-qPCR). SIRT2 was found to deacetylate NF-κB p65, inhibiting NLRP3 activation and reducing inflammatory cytokines. SIRT2 overexpression enhanced chondrocyte proliferation, DNA repair, and mitochondrial function while decreasing reactive oxygen species production. In vivo, SIRT2 significantly improved cartilage repair in OA mice with NLRP3 overexpression attenuating its protective effects. SIRT2 promotes cartilage repair in OA by regulating the NF-κB/NLRP3 axis, reducing inflammation and oxidative stress. This highlights SIRT2 as a potential therapeutic target for OA.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70031","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144550822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Nuclear binding SET domain 1 alleviates cartilage ferroptosis in knee osteoarthritis by upregulating the krüppel-like factor 9/autophagy-related 14 pathway via H3K36me2 modification 核结合SET结构域1通过H3K36me2修饰上调kr<s:1> ppel样因子9/自噬相关14通路，减轻膝关节骨性关节炎软骨铁吊

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-29 DOI: 10.1002/ccs3.70027

Qinglei Yang, Rugang Li, Zhiqiang Hu, Wengang Zhu, Hongying Yu

{"title":"Nuclear binding SET domain 1 alleviates cartilage ferroptosis in knee osteoarthritis by upregulating the krüppel-like factor 9/autophagy-related 14 pathway via H3K36me2 modification","authors":"Qinglei Yang, Rugang Li, Zhiqiang Hu, Wengang Zhu, Hongying Yu","doi":"10.1002/ccs3.70027","DOIUrl":"https://doi.org/10.1002/ccs3.70027","url":null,"abstract":"Knee osteoarthritis (KOA) is a progressive disease featured by cartilage damage. This study attempts to explore the role of nuclear binding SET domain 1 (NSD1) in KOA cartilage ferroptosis, thereby finding a new target for KOA treatment. Pathological changes, cartilage damage, and inflammatory cytokine levels in the established KOA mouse model were assessed. Primary mouse knee chondrocytes were separated, cultured, and challenged with IL-1β to establish in vitro KOA models. Cell viability was determined, Reactive oxygen species levels and ferroptosis-related factors were measured after interventions with NSD1, krüppel-like factor 9 (KLF9), and acyl-CoA synthetase long-chain family member 4 (ATG14). Furthermore, the enrichment of NSD1 and H3K36me2 on the KLF9 promoter as well as the enrichment of KLF9 on the ATG14 promoter was analyzed. Binding site between KLF9 and ATG14 promoter was assessed. NSD1 was downregulated in KOA mouse cartilage tissues and IL-1β-challenged chondrocytes. KOA severity was alleviated, chondrocyte viability was promoted, and ferroptosis was quenched after NSD1 overexpression. NSD1 strengthened H3K36me2 to upregulate KLF9 expression, and KLF9 transcriptionally activated ATG14 expression. KLF9 or ATG14 knockdown could both partially reverse the protective role of NSD1 overexpression on KOA cartilage ferroptosis. NSD1 enhanced KLF9 expression to improve ATG14 expression via H3K36me2 modification, thus relieving KOA cartilage ferroptosis.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144514678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Hypoxic adipose-derived stem cell exosomes as carriers of miR-100-5p to enhance angiogenesis and suppress inflammation in diabetic foot ulcers 低氧脂肪来源的干细胞外泌体作为miR-100-5p的载体，在糖尿病足溃疡中促进血管生成和抑制炎症

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-27 DOI: 10.1002/ccs3.70018

Hong Liu, Fei Hao, Bangtao Chen

{"title":"Hypoxic adipose-derived stem cell exosomes as carriers of miR-100-5p to enhance angiogenesis and suppress inflammation in diabetic foot ulcers","authors":"Hong Liu, Fei Hao, Bangtao Chen","doi":"10.1002/ccs3.70018","DOIUrl":"https://doi.org/10.1002/ccs3.70018","url":null,"abstract":"Diabetic foot ulcer (DFU) is a severe diabetes complication characterized by impaired angiogenesis and chronic inflammation, leading to delayed wound healing. Exosomes (Exo) derived from hypoxic adipose-derived stem cells (H-ADSCs-Exo) show potential as therapeutic carriers. This study investigates the role of H-ADSCs-Exo carrying miR-100-5p in DFU healing. ADSCs were isolated, characterized, and their Exo analyzed via transmission electron microscopy, nanoparticle tracking analysis, and Western blot. Transcriptome sequencing identified miR-100-5p as a key modulator of angiogenesis and inflammation. In vitro, H-ADSCs-Exo enhanced human umbilical vein endothelial cell and fibroblast proliferation, migration, and tube formation. In a rat DFU model, H-ADSCs-Exo administration reduced ulcer size, increased angiogenesis (VEGF/CD31 expression), and decreased inflammatory markers (TNF-α, IL-6). miR-100-5p overexpression further amplified these effects, demonstrating its critical role in Exo-mediated healing. These findings highlight the therapeutic potential of H-ADSCs-Exo in DFU treatment, offering insights into cell signaling mechanisms and paving the way for miRNA-based regenerative therapies.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144503000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

GRIN2B alleviates mid-gestational sevoflurane exposure-induced early differentiation of rat neural stem cells by interacting with KIF17 GRIN2B通过与KIF17相互作用减轻妊娠中期七氟醚暴露诱导的大鼠神经干细胞的早期分化

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-24 DOI: 10.1002/ccs3.70024

Mengyuan Li, Yan Hu, Zhonggui Cheng, Qianqian Li

{"title":"GRIN2B alleviates mid-gestational sevoflurane exposure-induced early differentiation of rat neural stem cells by interacting with KIF17","authors":"Mengyuan Li, Yan Hu, Zhonggui Cheng, Qianqian Li","doi":"10.1002/ccs3.70024","DOIUrl":"https://doi.org/10.1002/ccs3.70024","url":null,"abstract":"General anesthetic exposure during pregnancy has neurotoxic effects on the developing brain, causing long-term cognitive dysfunction in the offspring. Sevoflurane exposure during mid-gestation results in premature differentiation of neural stem cells (NSCs), being the crucial factor affecting normal hippocampal functions and contributing to neurocognitive impairment. However, the related molecular mechanism remains unclear. For in vivo assays, pregnant rats were exposed to 3% sevoflurane once on gestational day 14 (G14) or 3 times on G13, 14, and 15 (2 h per day). For in vitro assays, primary rat NSCs were isolated from fetal hippocampus tissues at 24 and 72 h after birth and on postnatal day 28. NSCs were transfected with GRIN2B or KIF17 overexpression plasmids before exposure to 4.1% sevoflurane for one or three consecutive days (2 h per day). Multiple sevoflurane exposures during the mid-trimester triggered NSC premature differentiation and decreased GRIN2B and KIF17 expression in the hippocampus of offspring rats and primary rat NSCs. GRIN2B or KIF17 overexpression attenuated sevoflurane-induced NSC premature differentiation. GRIN2B interacted with KIF17, and KIF17 silencing reversed the inhibition of GRIN2B overexpression on NSC early differentiation. GRIN2B alleviates NSC premature differentiation induced by repeated mid-gestational sevoflurane exposure via interaction with KIF17.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70024","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144472808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Naa10p impairs PGC-1α/Pparγ2 interaction to inhibit mitochondrial protection in pancreatitis Naa10p损害PGC-1α/Pparγ2相互作用，抑制胰腺炎线粒体保护

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-23 DOI: 10.1002/ccs3.70015

Jie Du, Hai Jiang, Taizhe Zhang, Chuanming Zheng, Zhong Ji

引用次数: 0

Cell line authentication and validation is a key requirement for Journal of Cell Communication and Signaling publications 细胞系认证和验证是《细胞通讯与信号》杂志出版物的关键要求

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-20 DOI: 10.1002/ccs3.70029

Ralf Weiskirchen, Jamie Almeida, Brahim Chaqour

{"title":"Cell line authentication and validation is a key requirement for Journal of Cell Communication and Signaling publications","authors":"Ralf Weiskirchen, Jamie Almeida, Brahim Chaqour","doi":"10.1002/ccs3.70029","DOIUrl":"https://doi.org/10.1002/ccs3.70029","url":null,"abstract":"Cell lines are essential tools in biomedical research and drug discovery, often substituting for tissues or organs of origin. However, frequent misidentification and cross-contamination pose major quality control challenges, leading to unreliable data, hindering scientific progress, and impacting clinical translation. Even authenticated cell lines may undergo genetic and phenotypic changes over time, affecting experimental outcomes. To promote transparency, reproducibility, and rigor, the Journal of Cell Communication and Signaling (JCCS) reaffirms its commitment to best practices in cell line authentication and validation, in alignment with Wiley's publishing ethics. Authors submitting manuscripts must provide comprehensive cell line details, including species, sex, tissue origin, name, and Research Resource Identifier. They are also required to document the source, acquisition date, and authentication methods such as short tandem repeat (STR) profiling and adventitious agent testing, including mycoplasma screening. By enforcing strict guidelines, JCCS seeks to improve research integrity, reduce erroneous findings, and enhance reproducibility. This initiative not only strengthens the reliability of published studies but also supports the broader scientific community in accelerating discovery and translating research into clinical advances for better human health.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70029","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144331926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Angio-associated migratory cell protein promotes colorectal cancer progression by enhancing phosphoglycerate kinase 1 phosphorylation 血管相关迁移细胞蛋白通过增强磷酸甘油酸激酶1磷酸化促进结直肠癌的进展

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-16 DOI: 10.1002/ccs3.70023

Wei Zhang, Qian Shi, Qincheng Liu, Haomiao Zhang, Ji Xia, Xueli Zhang

{"title":"Angio-associated migratory cell protein promotes colorectal cancer progression by enhancing phosphoglycerate kinase 1 phosphorylation","authors":"Wei Zhang, Qian Shi, Qincheng Liu, Haomiao Zhang, Ji Xia, Xueli Zhang","doi":"10.1002/ccs3.70023","DOIUrl":"https://doi.org/10.1002/ccs3.70023","url":null,"abstract":"To elucidate the oncogenic role of angio-associated migratory cell protein (AAMP) in colorectal cancer (CRC) and its mechanistic interplay with phosphoglycerate kinase 1 (PGK1). AAMP expression was analyzed in CRC and normal tissues (tissue microarrays-immunohistochemical/Western blot). Functional impacts were assessed via siRNA knockdown and lentiviral overexpression in CRC cell lines (proliferation: CCK-8/3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide/clonogenic assays; tumorigenesis: xenografts). Molecular mechanisms were explored through co-immunoprecipitation, phosphorylation assays, and Ribonucleic Acid (RNA) sequencing. AAMP was significantly upregulated in CRC versus normal tissues (p < 0.05), correlating with poor patient survival. AAMP knockdown suppressed CRC cell proliferation, colony formation, and xenograft tumor growth, whereas overexpression exacerbated these phenotypes. Mechanistically, AAMP directly bound PGK1 and enhanced its phosphorylation (p-PGK1), driving CRC proliferation. PGK1 silencing abrogated AAMP-mediated proliferative effects. RNA sequencing revealed AAMP modulation of immune-related pathways (Tumor Necrosis Factor, IL-17, Jak-STAT) and key proteins (EGFR, RPL10, NOD2), suggesting dual roles in proliferation. AAMP promotes CRC progression through PGK1 phosphorylation-dependent metabolic activation, proposing the AAMP-PGK1 axis as a therapeutic target for advanced CRC.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144299743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Modulation of podocyte extracellular matrix remodeling in membranous nephropathy by the NFATc3/LRRC55/BK channel pathway NFATc3/LRRC55/BK通道通路对膜性肾病足细胞细胞外基质重塑的调节

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-13 DOI: 10.1002/ccs3.70022

Yaling Guo, Jingliang Min, Baochao Chang, Lei Liu, Jiqiang Zhang, Weidong Chen

{"title":"Modulation of podocyte extracellular matrix remodeling in membranous nephropathy by the NFATc3/LRRC55/BK channel pathway","authors":"Yaling Guo, Jingliang Min, Baochao Chang, Lei Liu, Jiqiang Zhang, Weidong Chen","doi":"10.1002/ccs3.70022","DOIUrl":"https://doi.org/10.1002/ccs3.70022","url":null,"abstract":"Membranous nephropathy (MN) is a common glomerular disease characterized by podocyte injury. Although previous studies highlighted the leucine-rich repeat-containing 55/big potassium (LRRC55/BK) channel axis in Ang II-induced apoptosis, our study further investigates the upstream regulation by nuclear factor of activated T-cells 3 (NFATc3) and its role in extracellular matrix (ECM) remodeling. Using an Ang II-induced podocyte injury model, we found that NFATc3 overexpression promoted LRRC55 transcription, increased BK channel activity, and elevated intracellular calcium, thereby exacerbating podocyte apoptosis and impairing migration. RNA-seq and functional assays revealed significant upregulation of ECM-related genes, with enhanced fibronectin and collagen I deposition. Patch-clamp experiments confirmed BK channel activation was LRRC55-dependent. In vivo, NFATc3 knockdown attenuated renal injury, restored podocyte markers (nephrin, WT1, synaptopodin), and alleviated proteinuria and fibrosis, whereas LRRC55 overexpression or BK agonist NS1619 reversed these effects. These findings reveal that NFATc3 aggravates Ang II-induced podocyte injury through transcriptional regulation of LRRC55 and activation of the BK channel, contributing to ECM remodeling and glomerular dysfunction. Our results offer mechanistic insight into MN progression and suggest the NFATc3/LRRC55/BK axis as a potential therapeutic target.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144281463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Role of circ_0012856 in modulating molecular pathways of diabetic peripheral neuropathy circ_0012856在调节糖尿病周围神经病变分子通路中的作用

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-12 DOI: 10.1002/ccs3.70019

Ji Chen, Fan Zhang, Yangyuxi Chen, Yingqing Lu, Xinxin Liu, Yuanzhang Tang, Fengrui Yang

引用次数: 0