Cell Death and Differentiation最新文献_第10页

Correction to: Two hot spot mutant p53 mouse models display differential gain of function in tumorigenesis 更正：两种热点突变 p53 小鼠模型在肿瘤发生过程中显示出不同的功能增益。

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-09-10 DOI: 10.1038/s41418-024-01366-7

W. Hanel, N. Marchenko, S. Xu, S. Xiaofeng Yu, W. Weng, U. Moll

引用次数: 0

PHGDH/SYK: a hub integrating anti-fungal immunity and serine metabolism PHGDH/SYK：整合抗真菌免疫和丝氨酸代谢的枢纽

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-09-10 DOI: 10.1038/s41418-024-01374-7

Xinyong Zhang, Dongdong Hu, Xiaoyan Sun, Yichun Gu, Yong Zhou, Chuanxin Su, Shi Liu, Caiyan Zhang, Guoping Lu, Qiwen Wu, Aidong Chen

{"title":"PHGDH/SYK: a hub integrating anti-fungal immunity and serine metabolism","authors":"Xinyong Zhang, Dongdong Hu, Xiaoyan Sun, Yichun Gu, Yong Zhou, Chuanxin Su, Shi Liu, Caiyan Zhang, Guoping Lu, Qiwen Wu, Aidong Chen","doi":"10.1038/s41418-024-01374-7","DOIUrl":"10.1038/s41418-024-01374-7","url":null,"abstract":"Immune cells modify their metabolic pathways in response to fungal infections. Nevertheless, the biochemical underpinnings need to be better understood. This study reports that fungal infection drives a switch from glycolysis to the serine synthesis pathway (SSP) and one-carbon metabolism by inducing the interaction of spleen tyrosine kinase (SYK) and phosphoglycerate dehydrogenase (PHGDH). As a result, PHGDH promotes SYK phosphorylation, leading to the recruitment of SYK to C-type lectin receptors (CLRs). The CLR/SYK complex initiates signaling cascades that lead to transcription factor activation and pro-inflammatory cytokine production. SYK activates SSP and one-carbon metabolism by inducing PHGDH activity. Then, one-carbon metabolism supports S-adenosylmethionine and histone H3 lysine 36 trimethylation to drive the production of pro-inflammatory cytokines and chemokines. These findings reveal the crosstalk between amino acid metabolism, epigenetic modification, and CLR signaling during fungal infection.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"31 12","pages":"1664-1678"},"PeriodicalIF":13.7,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142160449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Foxk1 promotes bone formation through inducing aerobic glycolysis Foxk1 通过诱导有氧糖酵解促进骨形成。

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-09-05 DOI: 10.1038/s41418-024-01371-w

Chungeng Liu, Naibo Feng, Zhenmin Wang, Kangyan Zheng, Yongheng Xie, Hongyu Wang, Houqing Long, Songlin Peng

{"title":"Foxk1 promotes bone formation through inducing aerobic glycolysis","authors":"Chungeng Liu, Naibo Feng, Zhenmin Wang, Kangyan Zheng, Yongheng Xie, Hongyu Wang, Houqing Long, Songlin Peng","doi":"10.1038/s41418-024-01371-w","DOIUrl":"10.1038/s41418-024-01371-w","url":null,"abstract":"Transcription factor Foxk1 can regulate cell proliferation, differentiation, metabolism, and promote skeletal muscle regeneration and cardiogenesis. However, the roles of Foxk1 in bone formation is unknown. Here, we found that Foxk1 expression decreased in the bone tissue of aged mice and osteoporosis patients. Knockdown of Foxk1 in primary murine calvarial osteoblasts suppressed osteoblast differentiation and proliferation. Conditional knockout of Foxk1 in preosteoblasts and mature osteoblasts in mice exhibited decreased bone mass and mechanical strength due to reduced bone formation. Mechanistically, we identified Foxk1 targeted the promoter region of many genes of glycolytic enzyme by CUT&Tag analysis. Lacking of Foxk1 in primary murine calvarial osteoblasts resulted in reducing aerobic glycolysis. Inhibition of glycolysis by 2DG hindered osteoblast differentiation and proliferation induced by Foxk1 overexpression. Finally, specific overexpression of Foxk1 in preosteoblasts, driven by a preosteoblast specific osterix promoter, increased bone mass and bone mechanical strength of aged mice, which could be suppressed by inhibiting glycolysis. In summary, these findings reveal that Foxk1 plays a vital role in the osteoblast metabolism regulation and bone formation stimulation, offering a promising approach for preventing age-related bone loss.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"31 12","pages":"1650-1663"},"PeriodicalIF":13.7,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

A chromosome-coupled ubiquitin-proteasome pathway is required for meiotic surveillance 减数分裂监控需要染色体偶联泛素-蛋白酶体途径

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-09-05 DOI: 10.1038/s41418-024-01375-6

Ruirui Zhang, Bohan Liu, Yuqi Tian, Mingyu Xin, Qian Li, Xiuhua Huang, Yuanyuan Liu, Li Zhao, Feifei Qi, Ruoxi Wang, Xiaoqian Meng, Jianguo Chen, Jun Zhou, Jinmin Gao

{"title":"A chromosome-coupled ubiquitin-proteasome pathway is required for meiotic surveillance","authors":"Ruirui Zhang, Bohan Liu, Yuqi Tian, Mingyu Xin, Qian Li, Xiuhua Huang, Yuanyuan Liu, Li Zhao, Feifei Qi, Ruoxi Wang, Xiaoqian Meng, Jianguo Chen, Jun Zhou, Jinmin Gao","doi":"10.1038/s41418-024-01375-6","DOIUrl":"10.1038/s41418-024-01375-6","url":null,"abstract":"Defects in meiotic prophase can cause meiotic chromosome missegregation and aneuploid gamete formation. Meiotic checkpoints are activated in germ cells with meiotic defects, and cells with unfixed errors are eliminated by apoptosis. How such a surveillance process is regulated remains elusive. Here, we report that a chromosome-coupled ubiquitin-proteasome pathway (UPP) regulates meiotic checkpoint activation and promotes germ cell apoptosis in C. elegans meiosis-defective mutants. We identified an F-box protein, FBXL-2, that functions as a core component within the pathway. This chromosome-coupled UPP regulates meiotic DSB repair kinetics and chromosome dynamic behaviors in synapsis defective mutants. Disrupted UPP impairs the axial recruitment of the HORMA domain protein HIM-3, which is required for efficient germ cell apoptosis in synapsis defective mutants. Our data suggest that an efficient chromosome-coupled UPP functions as a part of the meiotic surveillance system by enhancing the integrity of the meiotic chromosome axis.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"31 12","pages":"1730-1745"},"PeriodicalIF":13.7,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142137989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Correction: Exosomal miR-101-3p and miR-423-5p inhibit medulloblastoma tumorigenesis through targeting FOXP4 and EZH2 更正：外泌体 miR-101-3p 和 miR-423-5p 通过靶向 FOXP4 和 EZH2 抑制髓母细胞瘤肿瘤发生。

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-09-04 DOI: 10.1038/s41418-024-01345-y

Ping Xue, Saihua Huang, Xiao Han, Caiyan Zhang, Lan Yang, Wenfeng Xiao, Jinrong Fu, Hao Li, Yufeng Zhou

引用次数: 0

Inhibition of inflammatory osteoclasts accelerates callus remodeling in osteoporotic fractures by enhancing CGRP+TrkA+ signaling 通过增强 CGRP+TrkA+ 信号，抑制炎性破骨细胞可加速骨质疏松性骨折的胼胝体重塑

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-09-02 DOI: 10.1038/s41418-024-01368-5

Yuexia Shu, Zhenyu Tan, Zhen Pan, Yujie Chen, Jielin Wang, Jieming He, Jia Wang, Yuan Wang

{"title":"Inhibition of inflammatory osteoclasts accelerates callus remodeling in osteoporotic fractures by enhancing CGRP+TrkA+ signaling","authors":"Yuexia Shu, Zhenyu Tan, Zhen Pan, Yujie Chen, Jielin Wang, Jieming He, Jia Wang, Yuan Wang","doi":"10.1038/s41418-024-01368-5","DOIUrl":"10.1038/s41418-024-01368-5","url":null,"abstract":"Impaired callus remodeling significantly contributes to the delayed healing of osteoporotic fractures; however, the underlying mechanisms remain unclear. Sensory neuronal signaling plays a crucial role in bone repair. In this study, we aimed to investigate the pathological mechanisms hindering bone remodeling in osteoporotic fractures, particularly focusing on the role of sensory neuronal signaling. We demonstrate that in ovariectomized (OVX) mice, the loss of CGRP+TrkA+ sensory neuronal signaling during callus remodeling correlates with increased Cx3cr1+iOCs expression within the bone callus. Conditional knockout of Cx3cr1+iOCs restored CGRP+TrkA+ sensory neuronal, enabling normal callus remodeling progression. Mechanistically, we further demonstrate that Cx3cr1+iOCs secrete Sema3A in the osteoporotic fracture repair microenvironment, inhibiting CGRP+TrkA+ sensory neurons’ axonal regeneration and suppressing nerve–bone signaling exchange, thus hindering bone remodeling. Lastly, in human samples, we observed an association between the loss of CGRP+TrkA+ sensory neuronal signaling and increased expression of Cx3cr1+iOCs. In conclusion, enhancing CGRP+TrkA+ sensory nerve signaling by inhibiting Cx3cr1+iOCs activity presents a potential strategy for treating delayed healing in osteoporotic fractures.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"31 12","pages":"1695-1706"},"PeriodicalIF":13.7,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41418-024-01368-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142118152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Publisher Correction: Cell death as an architect of adult skin stem cell niches 出版商更正：细胞死亡是成人皮肤干细胞龛的建筑师。

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-09-02 DOI: 10.1038/s41418-024-01362-x

Kim Lecomte, Annagiada Toniolo, Esther Hoste

引用次数: 0

LUBAC enables tumor-promoting LTβ receptor signaling by activating canonical NF-κB LUBAC 通过激活典型的 NF-κB 来实现促进肿瘤的 LTβ 受体信号转导

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-08-30 DOI: 10.1038/s41418-024-01355-w

Yu-Guang Chen, Eva Rieser, Amandeep Bhamra, Silvia Surinova, Peter Kreuzaler, Meng-Hsing Ho, Wen-Chiuan Tsai, Nieves Peltzer, Diego de Miguel, Henning Walczak

{"title":"LUBAC enables tumor-promoting LTβ receptor signaling by activating canonical NF-κB","authors":"Yu-Guang Chen, Eva Rieser, Amandeep Bhamra, Silvia Surinova, Peter Kreuzaler, Meng-Hsing Ho, Wen-Chiuan Tsai, Nieves Peltzer, Diego de Miguel, Henning Walczak","doi":"10.1038/s41418-024-01355-w","DOIUrl":"10.1038/s41418-024-01355-w","url":null,"abstract":"Lymphotoxin β receptor (LTβR), a member of the TNF receptor superfamily (TNFR-SF), is essential for development and maturation of lymphoid organs. In addition, LTβR activation promotes carcinogenesis by inducing a proinflammatory secretome. Yet, we currently lack a detailed understanding of LTβR signaling. In this study we discovered the linear ubiquitin chain assembly complex (LUBAC) as a previously unrecognized and functionally crucial component of the native LTβR signaling complex (LTβR-SC). Mechanistically, LUBAC-generated linear ubiquitin chains enable recruitment of NEMO, OPTN and A20 to the LTβR-SC, where they act coordinately to regulate the balance between canonical and non-canonical NF-κB pathways. Thus, different from death receptor signaling, where LUBAC prevents inflammation through inhibition of cell death, in LTβR signaling LUBAC is required for inflammatory signaling by enabling canonical and interfering with non-canonical NF-κB activation. This results in a LUBAC-dependent LTβR-driven inflammatory, protumorigenic secretome. Intriguingly, in liver cancer patients with high LTβR expression, high expression of LUBAC correlates with poor prognosis, providing clinical relevance for LUBAC-mediated inflammatory LTβR signaling.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"31 10","pages":"1267-1284"},"PeriodicalIF":13.7,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41418-024-01355-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142100896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Gelsolin alleviates rheumatoid arthritis by negatively regulating NLRP3 inflammasome activation 凝胶苷元通过负向调节 NLRP3 炎症小体的激活缓解类风湿性关节炎

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-08-24 DOI: 10.1038/s41418-024-01367-6

Jiyeon Lee, Fumiyuki Sasaki, Eri Koike, Minjeong Cho, Yeongun Lee, So Hee Dho, Jina Lee, Eunji Lee, Eri Toyohara, Mika Sunakawa, Mariko Ishibashi, Huynh Hiep Hung, Saki Nishioka, Ritsuko Komine, Chiaki Okura, Masumi Shimizu, Masahito Ikawa, Akihiko Yoshimura, Rimpei Morita, Lark Kyun Kim

{"title":"Gelsolin alleviates rheumatoid arthritis by negatively regulating NLRP3 inflammasome activation","authors":"Jiyeon Lee, Fumiyuki Sasaki, Eri Koike, Minjeong Cho, Yeongun Lee, So Hee Dho, Jina Lee, Eunji Lee, Eri Toyohara, Mika Sunakawa, Mariko Ishibashi, Huynh Hiep Hung, Saki Nishioka, Ritsuko Komine, Chiaki Okura, Masumi Shimizu, Masahito Ikawa, Akihiko Yoshimura, Rimpei Morita, Lark Kyun Kim","doi":"10.1038/s41418-024-01367-6","DOIUrl":"10.1038/s41418-024-01367-6","url":null,"abstract":"Despite numerous biomarkers being proposed for rheumatoid arthritis (RA), a gap remains in our understanding of their mechanisms of action. In this study, we discovered a novel role for gelsolin (GSN), an actin-binding protein whose levels are notably reduced in the plasma of RA patients. We elucidated that GSN is a key regulator of NLRP3 inflammasome activation in macrophages, providing a plausible explanation for the decreased secretion of GSN in RA patients. We found that GSN interacts with NLRP3 in LPS-primed macrophages, hence modulating the formation of the NLRP3 inflammasome complex. Reducing GSN expression significantly enhanced NLRP3 inflammasome activation. GSN impeded NLRP3 translocation to the mitochondria; it contributed to the maintenance of intracellular calcium equilibrium and mitochondrial stability. This maintenance is crucial for controlling the inflammatory response associated with RA. Furthermore, the exacerbation of arthritic symptoms in GSN-deficient mice indicates the potential of GSN as both a diagnostic biomarker and a therapeutic target. Moreover, not limited to RA models, GSN has demonstrated a protective function in diverse disease models associated with the NLRP3 inflammasome. Myeloid cell-specific GSN-knockout mice exhibited aggravated inflammatory responses in models of MSU-induced peritonitis, folic acid-induced acute tubular necrosis, and LPS-induced sepsis. These findings suggest novel therapeutic approaches that modulate GSN activity, offering promise for more effective management of RA and a broader spectrum of inflammatory conditions.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"31 12","pages":"1679-1694"},"PeriodicalIF":13.7,"publicationDate":"2024-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41418-024-01367-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142045556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Deficiency of thiosulfate sulfurtransferase mediates the dysfunction of renal tubular mitochondrial fatty acid oxidation in diabetic kidney disease 硫代硫酸硫基转移酶的缺乏介导了糖尿病肾病肾小管线粒体脂肪酸氧化的功能障碍。

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-08-22 DOI: 10.1038/s41418-024-01365-8

Jia Xiu Zhang, Pei Pei Chen, Xue Qi Li, Liang Li, Qin Yi Wu, Gui Hua Wang, Xiong Zhong Ruan, Kun Ling Ma

{"title":"Deficiency of thiosulfate sulfurtransferase mediates the dysfunction of renal tubular mitochondrial fatty acid oxidation in diabetic kidney disease","authors":"Jia Xiu Zhang, Pei Pei Chen, Xue Qi Li, Liang Li, Qin Yi Wu, Gui Hua Wang, Xiong Zhong Ruan, Kun Ling Ma","doi":"10.1038/s41418-024-01365-8","DOIUrl":"10.1038/s41418-024-01365-8","url":null,"abstract":"One of the main characteristics of diabetic kidney disease (DKD) is abnormal renal tubular fatty acid metabolism, especially defective fatty acid oxidation (FAO), accelerating tubular injury and tubulointerstitial fibrosis. Thiosulfate sulfurtransferase (TST), a mitochondrial enzyme essential for sulfur transfer, is reduced in metabolic diseases like diabetes and obesity. However, the potential role of TST in regulating fatty acid metabolic abnormalities in DKD remains unclear. Here, our data revealed decreased TST expression in the renal cortex of DKD patients. TST deficiency exacerbated tubular impairment in both diabetic and renal fibrosis mouse models, while sodium thiosulfate treatment or TST overexpression mitigated renal tubular injury with high-glucose exposure. TST downregulation mediated the decrease in S-sulfhydration of very long-chain specific acyl-CoA dehydrogenase, resulting in mitochondrial FAO dysfunction. This sequence of events exacerbates the progression of tubulointerstitial injury in DKD. Together, our findings demonstrate TST as a regulator of renal tubular injury in DKD.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"31 12","pages":"1636-1649"},"PeriodicalIF":13.7,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142016446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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