Cell Communication and Signaling最新文献

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Taurine can restrict MtdsRNA mediated pyroptosis by enhancing mitophagy in nucleus pulposus cells. 牛磺酸可以通过增强髓核细胞的自噬来抑制MtdsRNA介导的热凋亡。
IF 8.2 2区 生物学
Cell Communication and Signaling Pub Date : 2025-10-09 DOI: 10.1186/s12964-025-02431-5
Zixuan Ou, Junyu Wei, Bide Tong, Jie Lei, Huaizhen Liang, Dingchao Zhu, Hongchuan Wang, Xingyu Zhou, Di Wu, Hanpeng Xu, Zhi Du, Yifan Du, Shuchang Peng, Xiaoguang Zhang, Huipeng Yin, Kun Wang, Cao Yang, Zhiwei Liao
{"title":"Taurine can restrict MtdsRNA mediated pyroptosis by enhancing mitophagy in nucleus pulposus cells.","authors":"Zixuan Ou, Junyu Wei, Bide Tong, Jie Lei, Huaizhen Liang, Dingchao Zhu, Hongchuan Wang, Xingyu Zhou, Di Wu, Hanpeng Xu, Zhi Du, Yifan Du, Shuchang Peng, Xiaoguang Zhang, Huipeng Yin, Kun Wang, Cao Yang, Zhiwei Liao","doi":"10.1186/s12964-025-02431-5","DOIUrl":"https://doi.org/10.1186/s12964-025-02431-5","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"423"},"PeriodicalIF":8.2,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145260039","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}
引用次数: 0
Interactions between gut microbiota and parkinson's disease: the role of tryptophan metabolism. 肠道菌群与帕金森病之间的相互作用:色氨酸代谢的作用。
IF 8.2 2区 生物学
Cell Communication and Signaling Pub Date : 2025-10-09 DOI: 10.1186/s12964-025-02393-8
Xuemei Fan, Zhaoqun Xiao, Yan Chen, Hui Yang, Mengyuan Diao, Wei Hu, Shuai Wang
{"title":"Interactions between gut microbiota and parkinson's disease: the role of tryptophan metabolism.","authors":"Xuemei Fan, Zhaoqun Xiao, Yan Chen, Hui Yang, Mengyuan Diao, Wei Hu, Shuai Wang","doi":"10.1186/s12964-025-02393-8","DOIUrl":"https://doi.org/10.1186/s12964-025-02393-8","url":null,"abstract":"<p><p>Parkinson's disease, a common neurodegenerative disorder in the elderly, is characterized by motor symptoms and non-motor symptoms such as anxiety, depression, sleep disturbances, and gastrointestinal dysfunction, highlighting its nature as a multisystem disease. The critical role of the microbiota-gut-brain axis in maintaining human homeostasis is well established, and growing evidence links its dysfunction and gut microbiota dysbiosis to Parkinson's disease. Communication between the microbiota and the brain occurs through various pathways, including the vagus nerve, intestinal hormonal signals, the immune system, tryptophan metabolism, and microbial metabolites. Among these, tryptophan metabolism is a key metabolic pathway. As an essential amino acid that animal cells cannot synthesize, tryptophan and its metabolites in the intestine depend entirely on dietary intake and gut microbiota production. In the gastrointestinal tract, tryptophan metabolism occurs via three main pathways-the indole pathway, the kynurenine pathway, and the serotonin pathway-all directly or indirectly regulated by gut microbiota. These metabolites are vital in mediating the 'microbiota-gut-brain' dialogue and regulating gastrointestinal functions. Additionally, some metabolites mediate central nervous system inflammation and contribute to neurodegenerative disease processes as aromatic hydrocarbon receptor ligands. This review examines recent research on gut microbiota and host tryptophan co-metabolism and their roles in the development of Parkinson's disease. Furthermore, it explores how targeting gut microbiota and modulating tryptophan metabolism could offer potential therapeutic approaches for Parkinson's disease.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"424"},"PeriodicalIF":8.2,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145259790","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}
引用次数: 0
Septins in the nervous system: from cytoskeletal dynamics to neurological disorders. 神经系统中的蛋白酶:从细胞骨架动力学到神经系统疾病。
IF 8.2 2区 生物学
Cell Communication and Signaling Pub Date : 2025-10-09 DOI: 10.1186/s12964-025-02430-6
Rayyah R Alkhanjari, Maitha M Alhajeri, Poorna Manasa Bhamidimarri, Khalood Alhosani, Junaid Kashir, Tomohiro Torii, Hamdan Hamdan
{"title":"Septins in the nervous system: from cytoskeletal dynamics to neurological disorders.","authors":"Rayyah R Alkhanjari, Maitha M Alhajeri, Poorna Manasa Bhamidimarri, Khalood Alhosani, Junaid Kashir, Tomohiro Torii, Hamdan Hamdan","doi":"10.1186/s12964-025-02430-6","DOIUrl":"https://doi.org/10.1186/s12964-025-02430-6","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"425"},"PeriodicalIF":8.2,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145260005","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}
引用次数: 0
The impact of post-translational modifications and subcellular localization on NLRP3 inflammasome activation: A systematic review. 翻译后修饰和亚细胞定位对NLRP3炎性体激活的影响:系统综述。
IF 8.2 2区 生物学
Cell Communication and Signaling Pub Date : 2025-10-09 DOI: 10.1186/s12964-025-02426-2
Shuchi Zhang, Muhammad Usman, Qianxi Wu, Yingjie Gao, Lifeng Fu, Maoping Chu, Chang Jia
{"title":"The impact of post-translational modifications and subcellular localization on NLRP3 inflammasome activation: A systematic review.","authors":"Shuchi Zhang, Muhammad Usman, Qianxi Wu, Yingjie Gao, Lifeng Fu, Maoping Chu, Chang Jia","doi":"10.1186/s12964-025-02426-2","DOIUrl":"https://doi.org/10.1186/s12964-025-02426-2","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"426"},"PeriodicalIF":8.2,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145260008","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}
引用次数: 0
Extracellular matrix protein signaling promotes multi-step cancer vasculogenic mimicry formation. 细胞外基质蛋白信号传导促进多步骤癌症血管模拟形成。
IF 8.2 2区 生物学
Cell Communication and Signaling Pub Date : 2025-10-08 DOI: 10.1186/s12964-025-02428-0
Gabriel Mingo, Andrés Valdivia, Gema Nicolle Santander, Nicole Babbitt, Varina Aldana, Javiera Pradenas, Pamela González, Cristóbal Canales, Jorge A Toledo, Carolina Ibáñez, Francisco Nualart, Manuel Varas-Godoy, Roger Gejman, Juan Carlos Roa, Andrea Ravasio, Cristina Bertocchi, Gareth I Owen
{"title":"Extracellular matrix protein signaling promotes multi-step cancer vasculogenic mimicry formation.","authors":"Gabriel Mingo, Andrés Valdivia, Gema Nicolle Santander, Nicole Babbitt, Varina Aldana, Javiera Pradenas, Pamela González, Cristóbal Canales, Jorge A Toledo, Carolina Ibáñez, Francisco Nualart, Manuel Varas-Godoy, Roger Gejman, Juan Carlos Roa, Andrea Ravasio, Cristina Bertocchi, Gareth I Owen","doi":"10.1186/s12964-025-02428-0","DOIUrl":"https://doi.org/10.1186/s12964-025-02428-0","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"422"},"PeriodicalIF":8.2,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145253786","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}
引用次数: 0
LIMCH1 inhibits antitumor immunity by upregulating PDL1 in triple-negative breast cancer. LIMCH1在三阴性乳腺癌中通过上调PDL1抑制抗肿瘤免疫。
IF 8.2 2区 生物学
Cell Communication and Signaling Pub Date : 2025-10-08 DOI: 10.1186/s12964-025-02387-6
Minghan Qiu, Zhanhua Gao, Mengran Tian, Yuya Liu, Jinpu Liu, Qiaonan Zhang, Ruxue Liu, Yayun Wang, Xiangqian Zheng, Jie Hao, Zhen Yang, Ming Gao
{"title":"LIMCH1 inhibits antitumor immunity by upregulating PDL1 in triple-negative breast cancer.","authors":"Minghan Qiu, Zhanhua Gao, Mengran Tian, Yuya Liu, Jinpu Liu, Qiaonan Zhang, Ruxue Liu, Yayun Wang, Xiangqian Zheng, Jie Hao, Zhen Yang, Ming Gao","doi":"10.1186/s12964-025-02387-6","DOIUrl":"https://doi.org/10.1186/s12964-025-02387-6","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"419"},"PeriodicalIF":8.2,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145253740","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}
引用次数: 0
BMAL1 modulation alleviates inflammatory responses in monocytes by targeting the Fis1-mediated mitochondrial unfolded protein response in high-altitude hypoxia. BMAL1调节通过靶向高海拔缺氧条件下fis1介导的线粒体未折叠蛋白反应来缓解单核细胞的炎症反应。
IF 8.2 2区 生物学
Cell Communication and Signaling Pub Date : 2025-10-08 DOI: 10.1186/s12964-025-02420-8
Yi-Ling Ge, Jin Xu, Yue Cai, Bin Zhang, Si-Yuan He, Pei-Jie Li, Ying-Rui Bu, Lin Zhang, Zhi-Bin Yu, Heng Ma, Yong Liu, Xiong-Wen Chen, Man-Jiang Xie
{"title":"BMAL1 modulation alleviates inflammatory responses in monocytes by targeting the Fis1-mediated mitochondrial unfolded protein response in high-altitude hypoxia.","authors":"Yi-Ling Ge, Jin Xu, Yue Cai, Bin Zhang, Si-Yuan He, Pei-Jie Li, Ying-Rui Bu, Lin Zhang, Zhi-Bin Yu, Heng Ma, Yong Liu, Xiong-Wen Chen, Man-Jiang Xie","doi":"10.1186/s12964-025-02420-8","DOIUrl":"https://doi.org/10.1186/s12964-025-02420-8","url":null,"abstract":"<p><strong>Background: </strong>Hypoxia-induced inflammation has been implicated in the progression of high-altitude illnesses. Mitochondria are key organelles for oxygen metabolism and inflammation that are controlled by circadian clocks. However, little is known regarding how circadian clocks sense hypoxic signals and trigger downstream mitochondrial responses.</p><p><strong>Methods: </strong>Human participants and mice were exposed to a real or simulated high-altitude setting of 5500 m. Multichannel fluorescence intravital microscopy was used for in vivo molecular imaging of inflammation. Bioinformatics analysis, myeloid-specific knockout mice, and RAW 264.7 cells were used to investigate the underlying inflammatory mechanisms.</p><p><strong>Results: </strong>We found that high-altitude hypoxia induced dynamic inflammatory activity in monocytes, characterized by significantly increased levels of cytokines (interleukin-6 [IL-6], IL-1β and monocyte chemoattractant protein-1) after acute (3-day) exposure, which returned to control levels after a prolonged (30-day) exposure. Bioinformatics analysis revealed that the core circadian transcription factor brain and muscle Arnt-like 1 (BMAL1) correlated positively with hypoxia-induced inflammation in monocytes. Mechanistically, BMAL1 induced NOD-like receptor protein 3 inflammasome activation in monocytes by targeting the Fis1-mediated mitochondrial unfolded protein response. Basic helix-loop-helix family member E40, a hypoxic stress-responsive transcription factor, directly promoted Bmal1 transcription and triggered inflammation in monocytes. In contrast, myeloid-specific deletion of BMAL1 alleviated the inflammatory activity of monocytes and circulating inflammation, both in vitro and in vivo, under high-altitude hypoxia.</p><p><strong>Conclusions: </strong>Our findings indicate that transcriptional activation of Bmal1 in monocytes can potentially serve as a novel biomarker of hypoxia-induced inflammation. Our findings also suggest a novel approach for modulating the intrinsic clock, which might render organisms less vulnerable to high-altitude hypoxia.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"420"},"PeriodicalIF":8.2,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145253717","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}
引用次数: 0
Ototoxicity-induced c-Fos activation underlies the regenerative capacity of the vestibular sensory epithelia. 耳毒性诱导的c-Fos激活是前庭感觉上皮再生能力的基础。
IF 8.2 2区 生物学
Cell Communication and Signaling Pub Date : 2025-10-08 DOI: 10.1186/s12964-025-02446-y
Yunzhong Zhang, Dan You, Chenhao Che, Xinyuan Wang, Huawei Li, Yi-Quan Tang, Shan Sun
{"title":"Ototoxicity-induced c-Fos activation underlies the regenerative capacity of the vestibular sensory epithelia.","authors":"Yunzhong Zhang, Dan You, Chenhao Che, Xinyuan Wang, Huawei Li, Yi-Quan Tang, Shan Sun","doi":"10.1186/s12964-025-02446-y","DOIUrl":"https://doi.org/10.1186/s12964-025-02446-y","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"421"},"PeriodicalIF":8.2,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145253832","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}
引用次数: 0
Endothelial cell-derived apoptotic bodies modulate innate and adaptive immune responses during inflammation. 内皮细胞衍生的凋亡小体在炎症期间调节先天和适应性免疫反应。
IF 8.2 2区 生物学
Cell Communication and Signaling Pub Date : 2025-10-07 DOI: 10.1186/s12964-025-02382-x
Caitlin L Vella, Pamali Fonseka, Emma J Grant, Stephanie F Rutter, Donia Y Abeid, Dilara C Ozkocak, Tien K Nguyen, Antony Vinh, Stephanie Paone, Grant R Drummond, Christopher G Sobey, Stephanie Gras, Mark D Hulett, Suresh Mathivanan, Ivan K H Poon, Amy A Baxter
{"title":"Endothelial cell-derived apoptotic bodies modulate innate and adaptive immune responses during inflammation.","authors":"Caitlin L Vella, Pamali Fonseka, Emma J Grant, Stephanie F Rutter, Donia Y Abeid, Dilara C Ozkocak, Tien K Nguyen, Antony Vinh, Stephanie Paone, Grant R Drummond, Christopher G Sobey, Stephanie Gras, Mark D Hulett, Suresh Mathivanan, Ivan K H Poon, Amy A Baxter","doi":"10.1186/s12964-025-02382-x","DOIUrl":"10.1186/s12964-025-02382-x","url":null,"abstract":"<p><p>Endothelial cells (ECs) act as gatekeepers and signalling hubs that coordinate communication between blood vessels and surrounding tissues by regulating vascular tone, immune responses and numerous other physiological processes. During vascular inflammation commonly associated with aging, atherosclerosis, diabetes and autoimmunity, a range of biological, environmental and physical stressors can induce activation and apoptosis of ECs. Apoptotic bodies (ApoBDs) are large (~ 1-5 μm), membrane‑bound extracellular vesicles generated solely through apoptotic cell disassembly, that are increasingly recognised as mediators of intercellular communication via the transfer of bioactive molecules to target cells. Although EC apoptosis is a central feature of vascular inflammatory disorders, the formation of EC‑derived ApoBDs and their immunomodulatory roles when formed in an inflammatory environment, remains poorly defined. This study aimed to characterise the functional properties of EC‑derived ApoBDs generated under inflammatory conditions in vitro. A proteomics analysis of EC‑derived ApoBDs revealed that EC‑ApoBDs generated during inflammation ('iApoBDs') were enriched in inflammatory cytokines/chemokines, adhesion molecules and antigen presentation machinery compared with non-inflammatory ('ApoBD') controls. Functionally, iApoBDs promoted monocyte chemotaxis via the release of MCP-1, while altered expression of the adhesion molecule ICAM-1 enhanced efferocytosis by macrophages in vitro and in vivo. Furthermore, iApoBDs generated from antigen-pulsed HUVECs promoted IFN‑𝛾 expression by peptide specific CD8 T cells in an in vitro model of antigen presentation. These findings demonstrate that within an inflammatory setting, apoptotic ECs can participate in continued communication with their environment via the generation of ApoBDs, thereby modulating innate and adaptive immune processes. The formation of ApoBDs by ECs may serve as a target for therapeutic interventions in inflammatory vascular diseases.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"418"},"PeriodicalIF":8.2,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12502297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145245848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Tubacin alleviate the reproductive toxicity of deoxynivalenol in mouse oocytes and zygotes via strengthening microtubule stability. Tubacin通过增强微管稳定性减轻脱氧雪腐镰刀菌醇对小鼠卵母细胞和受精卵的生殖毒性。
IF 8.2 2区 生物学
Cell Communication and Signaling Pub Date : 2025-10-03 DOI: 10.1186/s12964-025-02432-4
Hui Luo, Jianhua Chen, Zhihan Guo, Yanyan Zhu, Yipin Wang, Tian Wu, Siyue Yin, Cao Li, Youqiang Su, Yao Chen, Yun Qian, Congxiu Miao, Ruizhi Feng
{"title":"Tubacin alleviate the reproductive toxicity of deoxynivalenol in mouse oocytes and zygotes via strengthening microtubule stability.","authors":"Hui Luo, Jianhua Chen, Zhihan Guo, Yanyan Zhu, Yipin Wang, Tian Wu, Siyue Yin, Cao Li, Youqiang Su, Yao Chen, Yun Qian, Congxiu Miao, Ruizhi Feng","doi":"10.1186/s12964-025-02432-4","DOIUrl":"10.1186/s12964-025-02432-4","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"417"},"PeriodicalIF":8.2,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145226238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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