Cell Death Discovery最新文献_第3页

Mitophagy: insights into its signaling molecules, biological functions, and therapeutic potential in breast cancer. 有丝分裂：对其信号分子、生物功能和乳腺癌治疗潜力的深入研究。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2024-10-29 DOI: 10.1038/s41420-024-02226-6

Cong Chen, Aizhai Xiang, Xia Lin, Jufeng Guo, Jian Liu, Shufang Hu, Tao Rui, Qianwei Ye

引用次数: 0

Nr1d1 inhibition mitigates intermittent hypoxia-induced pulmonary hypertension via Dusp1-mediated Erk1/2 deactivation and mitochondrial fission attenuation. 抑制 Nr1d1 可通过 Dusp1 介导的 Erk1/2 失活和线粒体裂变衰减缓解间歇性缺氧诱发的肺动脉高压。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2024-10-29 DOI: 10.1038/s41420-024-02219-5

Zhou Pan, Yan Yao, Xu Liu, Yixuan Wang, Xinyue Zhang, Shiqian Zha, Ke Hu

{"title":"Nr1d1 inhibition mitigates intermittent hypoxia-induced pulmonary hypertension via Dusp1-mediated Erk1/2 deactivation and mitochondrial fission attenuation.","authors":"Zhou Pan, Yan Yao, Xu Liu, Yixuan Wang, Xinyue Zhang, Shiqian Zha, Ke Hu","doi":"10.1038/s41420-024-02219-5","DOIUrl":"10.1038/s41420-024-02219-5","url":null,"abstract":"Intermittent hypoxia (IH) precipitates pulmonary vasoconstriction, culminating in the onset of pulmonary hypertension (PH) among individuals afflicted with sleep apnea. While Nuclear receptor subfamily 1 group D member 1 (Nr1d1) is progressively recognized as pivotal regulator of cellular physiology, the role in the pathogenesis of IH-induced PH remains largely uncharted. The expression of Nr1d1 was examined in IH-induced rodent PH and in IH-treated PASMCs. To elucidate the contribution of Nr1d1 to the development of IH-induced PH, we employed siRNA to modulate Nr1d1 expression in vitro and employed serotype 1 adeno-associated virus (AAV1) in vivo. Nr1d1 levels were elevated in IH-induced rodents PH lung tissues and IH-treated PASMCs. Knocking down Nr1d1 by AAV1 effectively inhibited PH progression in chronic IH-induced PH models. Mechanistic investigations identified dual specificity phosphatase 1 (Dusp1), as a direct target that Nr1d1 trans-repressed, mediating Nr1d1's regulatory influence on Erk1/2/Drp1 signaling. Nr1d1 deficiency ameliorates mitochondrial dysfunction and fission by restoring Dusp1 dysregulation and Drp1 phosphorylation. Activation of Erk1/2 with PMA reversed the Dusp1-mediated regulation of Drp1 phosphorylation, indicating the involvement of the Erk1/2 pathway in Drp1 phosphorylation controlled by Dusp1. Meanwhile, intermittent hypoxia induced more severe PH in Dusp1 knockout mice compared with wild-type mice. Our data unveil a novel role for Nr1d1 in IH-induced PH pathogenesis and an undisclosed Nr1d1-Dusp1 axis in PASMCs mitochondrial fission regulation.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"10 1","pages":"459"},"PeriodicalIF":6.1,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11522549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544033","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

Unraveling the landscape of m6A RNA methylation in wound healing and scars. 揭开伤口愈合和疤痕中 m6A RNA 甲基化的面纱。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2024-10-29 DOI: 10.1038/s41420-024-02222-w

Qi Zhang, Liming Dong, Song Gong, Ting Wang

{"title":"Unraveling the landscape of m6A RNA methylation in wound healing and scars.","authors":"Qi Zhang, Liming Dong, Song Gong, Ting Wang","doi":"10.1038/s41420-024-02222-w","DOIUrl":"10.1038/s41420-024-02222-w","url":null,"abstract":"Wound healing is a complex process involving sequential stages of hemostasis, inflammation, proliferation, and remodeling. Multiple cell types and factors, including underlying conditions like diabetes and bacterial colonization, can influence healing outcomes and scar formation. N6-methyladenosine (m6A), a predominant RNA modification, plays crucial roles in gene expression regulation, impacting various biological processes and diseases. m6A regulates embryonic skin morphogenesis, wound repair, and pathophysiological processes like inflammation and angiogenesis. Recent studies have highlighted the role of m6A in wound healing, scar formation, and tissue remodeling. Additionally, m6A presents a unique expression pattern in pathological wounds and scars, potentially influencing wound healing and scar formation through modulating gene expression and cellular signaling, thereby serving as potential biomarkers or therapeutic targets. Targeting m6A modifications are potential strategies to enhance wound healing and reduce scar formation. This review aims to explore the roles and mechanisms of m6A RNA methylation in wound healing and scars, and discuss current challenges and perspectives. Continued research in this field will provide significant value for optimal wound repair and scar treatment.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"10 1","pages":"458"},"PeriodicalIF":6.1,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11522467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544035","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

Quantitative chemical proteomics reveals that phenethyl isothiocyanate covalently targets BID to promote apoptosis. 定量化学蛋白质组学揭示了异硫氰酸苯乙酯可共价作用于 BID，从而促进细胞凋亡。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2024-10-29 DOI: 10.1038/s41420-024-02225-7

Xiaoshu Dong, Xinqian Yu, Minghao Lu, Yaxin Xu, Liyan Zhou, Tao Peng

{"title":"Quantitative chemical proteomics reveals that phenethyl isothiocyanate covalently targets BID to promote apoptosis.","authors":"Xiaoshu Dong, Xinqian Yu, Minghao Lu, Yaxin Xu, Liyan Zhou, Tao Peng","doi":"10.1038/s41420-024-02225-7","DOIUrl":"10.1038/s41420-024-02225-7","url":null,"abstract":"Naturally occurring isothiocyanates (ITCs) found in cruciferous vegetables, such as benzyl isothiocyanate (BITC), phenethyl isothiocyanate (PEITC), and sulforaphane (SFN), have attracted significant research interest for their promising anti-cancer activity in vitro and in vivo. While the induction of apoptosis is recognized to play a key role in the anti-cancer effects of ITCs, the specific protein targets and associated upstream events underlying ITC-induced apoptosis remain unknown. In this study, we present a set of chemical probes that are derived from BITC, PEITC, and SFN and equipped with bioorthogonal alkynyl handles to systematically profile the target proteins of ITCs in live cancer cells. Using a competition-based quantitative chemical proteomics approach, we identify a range of candidate target proteins of ITCs enriched in biological processes such as apoptosis. We show that BID, an apoptosis regulator of the Bcl-2 family, is covalently modified by ITCs on its N-terminal cysteines. Functional characterization demonstrates that covalent binding to N-terminal cysteines of BID by PEITC results in conformational changes of the protein and disruption of the self-inhibitory interaction between N- and C-terminal regions of BID, thus unleashing the highly active C-terminal segment to exert downstream pro-apoptotic effects. Consistently, PEITC promotes the cleavage and mitochondrial translocation of BID, leading to a strong induction of apoptosis. We further show that mutation of N-terminal cysteines impairs the N- and C-terminal interaction of BID, relieving the self-inhibition and enhancing its apoptotic activity. Overall, our chemical proteomics profiling and functional studies not only reveal BID as the principal target of PEITC in mediating upstream events for the induction of apoptosis, but also uncover a novel molecular mechanism involving N-terminal cysteines within the first helix of BID in regulating its pro-apoptotic potential.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"10 1","pages":"456"},"PeriodicalIF":6.1,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11522290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544034","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

Xanthohumol overcomes osimertinib resistance via governing ubiquitination-modulated Ets-1 turnover. 黄腐醇通过调节泛素化调控的Ets-1周转克服奥希替尼耐药性

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2024-10-28 DOI: 10.1038/s41420-024-02220-y

Ying Ma, Ruirui Wang, Jinzhuang Liao, Pengfei Guo, Qiang Wang, Wei Li

{"title":"Xanthohumol overcomes osimertinib resistance via governing ubiquitination-modulated Ets-1 turnover.","authors":"Ying Ma, Ruirui Wang, Jinzhuang Liao, Pengfei Guo, Qiang Wang, Wei Li","doi":"10.1038/s41420-024-02220-y","DOIUrl":"10.1038/s41420-024-02220-y","url":null,"abstract":"Non-small cell lung cancer (NSCLC) is a prevalent and fatal malignancy with a significant global impact. Recent advancements have introduced targeted therapies like tyrosine kinase inhibitors (TKIs) such as osimertinib, which have improved patient outcomes, particularly in those with EGFR mutations. Despite these advancements, acquired resistance to TKIs remains a significant challenge. Hence, one of the current research priorities is understanding the resistance mechanisms and identifying new therapeutic targets to improve therapeutic efficacy. Herein, we identified high expression of c-Met in osimertinib-resistant NSCLC cells, and depletion of c-Met significantly inhibited the proliferation of osimertinib-resistant cells and prolonged survival in mice, suggesting c-Met as an attractive therapeutic target. To identify effective anti-tumor agents targeting c-Met, we screened a compound library containing 641 natural products and found that only xanthohumol exhibited potent inhibitory effects against osimertinib-resistant NSCLC cells. Moreover, combination treatment with xanthohumol and osimertinib sensitized osimertinib-resistant NSCLC cells to osimertinib both in vitro and in vivo. Mechanistically, xanthohumol disrupted the interaction between USP9X and Ets-1, and inhibited the phosphorylation of Ets-1 at Thr38, promoting its degradation, thereby targeting the Ets-1/c-Met signaling axis and inducing intrinsic apoptosis in osimertinib-resistant NSCLC cells. Overall, the research highlights the critical role of targeting c-Met to address osimertinib resistance in NSCLC. By demonstrating the efficacy of xanthohumol in overcoming resistance and enhancing therapeutic outcomes, this study provides valuable insights and potential new strategies for improving the clinical management of NSCLC.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"10 1","pages":"454"},"PeriodicalIF":6.1,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11519634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521146","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

The mechanisms behind heatstroke-induced intestinal damage. 中暑诱发肠道损伤的机制。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2024-10-28 DOI: 10.1038/s41420-024-02210-0

Minshu Sun, Qin Li, Zhimin Zou, Jian Liu, Zhengtao Gu, Li Li

{"title":"The mechanisms behind heatstroke-induced intestinal damage.","authors":"Minshu Sun, Qin Li, Zhimin Zou, Jian Liu, Zhengtao Gu, Li Li","doi":"10.1038/s41420-024-02210-0","DOIUrl":"10.1038/s41420-024-02210-0","url":null,"abstract":"With the frequent occurrence of heatwaves, heatstroke (HS) is expected to become one of the main causes of global death. Being a multi-organized disease, HS can result in circulatory disturbance and systemic inflammatory response, with the gastrointestinal tract being one of the primary organs affected. Intestinal damage plays an initiating and promoting role in HS. Multiple pathways result in damage to the integrity of the intestinal epithelial barrier due to heat stress and hypoxia brought on by blood distribution. This usually leads to intestinal leakage as well as the infiltration and metastasis of toxins and pathogenic bacteria in the intestinal cavity, which will eventually cause inflammation in the whole body. A large number of studies have shown that intestinal damage after HS involves the body's stress response, disruption of oxidative balance, disorder of tight junction proteins, massive cell death, and microbial imbalance. Based on these damage mechanisms, protecting the intestinal barrier and regulating the body's inflammatory and immune responses are effective treatment strategies. To better understand the pathophysiology of this complex process, this review aims to outline the potential processes and possible therapeutic strategies for intestinal damage after HS in recent years.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"10 1","pages":"455"},"PeriodicalIF":6.1,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11519599/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521145","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

CDK4/6 inhibition initiates cell cycle arrest by nuclear translocation of RB and induces a multistep molecular response. CDK4/6 抑制通过 RB 的核转位启动细胞周期停滞，并诱发多步分子反应。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2024-10-26 DOI: 10.1038/s41420-024-02218-6

Ting Hong, Anna C Hogger, Dongbiao Wang, Qi Pan, Julie Gansel, Thomas Engleitner, Rupert Öllinger, Jürgen E Gschwend, Roland Rad, Roman Nawroth

{"title":"CDK4/6 inhibition initiates cell cycle arrest by nuclear translocation of RB and induces a multistep molecular response.","authors":"Ting Hong, Anna C Hogger, Dongbiao Wang, Qi Pan, Julie Gansel, Thomas Engleitner, Rupert Öllinger, Jürgen E Gschwend, Roland Rad, Roman Nawroth","doi":"10.1038/s41420-024-02218-6","DOIUrl":"10.1038/s41420-024-02218-6","url":null,"abstract":"CDK4/6 inhibitors are standard of care in the treatment of metastatic breast cancer. Treatment regimen consists of a combination with endocrine therapy, since their therapeutic efficacy as monotherapy in most clinical trials was rather limited. Thus, understanding the molecular mechanisms that underlie response to therapy might allow for the development of an improved therapy design. We analyzed the response to the CDK4/6 inhibitor palbociclib in bladder cancer cells over a 48-hour time course using RNA sequencing and identified a multi-step mechanism of response. We next translated these results to the molecular mechanism in bladder cancer cells upon PD treatment. The initial step is characterized by translocation of the RB protein into the nucleus by activation of importin α/β, a mechanism that requires the NLS sequence. In parallel, RB is proteolyzed in the cytoplasm, a process regulated by gankyrin and the SCF complex. Only hypophosphorylated RB accumulates in the nucleus, which is an essential step for an efficient therapy response by initiating G1 arrest. This might explain the poor response in RB negative or mutated patients. At later stages during therapy, increased expression of the MiT/TFE protein family leads to lysosomal biogenesis which is essential to maintain this response. Lastly, cancer cells either undergo senescence and apoptosis or develop mechanisms of resistance following CDK4/6 inhibition.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"10 1","pages":"453"},"PeriodicalIF":6.1,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11513128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495898","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

The oncogenic axis YAP/MYC/EZH2 impairs PTEN tumor suppression activity enhancing lung tumorigenicity. 致癌轴YAP/MYC/EZH2损害了PTEN的肿瘤抑制活性，从而增强了肺癌的致病性。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2024-10-25 DOI: 10.1038/s41420-024-02216-8

Federica Lo Sardo, Chiara Turco, Beatrice Messina, Andrea Sacconi, Francesca Romana Auciello, Claudio Pulito, Sabrina Strano, Sima Lev, Giovanni Blandino

{"title":"The oncogenic axis YAP/MYC/EZH2 impairs PTEN tumor suppression activity enhancing lung tumorigenicity.","authors":"Federica Lo Sardo, Chiara Turco, Beatrice Messina, Andrea Sacconi, Francesca Romana Auciello, Claudio Pulito, Sabrina Strano, Sima Lev, Giovanni Blandino","doi":"10.1038/s41420-024-02216-8","DOIUrl":"https://doi.org/10.1038/s41420-024-02216-8","url":null,"abstract":"The tumor suppressor PTEN (phosphatase and tensin homolog deleted in chromosome 10) is genetically deleted or downregulated in many cancer types. Loss of PTEN protein expression is frequently found in lung cancer while genetic alterations are less abundant. PTEN expression is regulated at multiple genetic and epigenetic levels and even partial reduction of its expression increases cancer occurrence. We show that YAP and TAZ cooperate with EZH2, and MYC to transcriptionally repress onco-suppressor genes, including PTEN, in non-small cell lung cancer (NSCLC) cells. YAP/TAZ-EZH2-MYC transcriptional regulators form a nuclear complex that represses PTEN transcription, while their combinatorial targeting restores PTEN expression, attenuates NSCLC cell growth, and prevents compensatory responses induced by single treatments. Datasets analysis of NSCLC patients revealed that PTEN expression is negatively correlated to YAP/TAZ, EZH2 and MYC and that low expression of PTEN is predictive of poor prognosis, especially at earlier stages of the disease. These findings highlight the repressive role of the YAP/TAZ-EZH2-MYC axis on tumor-suppressor genes and offer a potential therapeutic strategy for lung cancer patients with low PTEN levels.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"10 1","pages":"452"},"PeriodicalIF":6.1,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11511861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495902","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

Deciphering the nexus between long non-coding RNAs and endoplasmic reticulum stress in hepatocellular carcinoma: biomarker discovery and therapeutic horizons. 解密肝细胞癌中长非编码 RNA 与内质网应激之间的关系：生物标记物的发现与治疗前景。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2024-10-24 DOI: 10.1038/s41420-024-02200-2

Himanshi Goyal, Sachin Parwani, Jyotdeep Kaur

{"title":"Deciphering the nexus between long non-coding RNAs and endoplasmic reticulum stress in hepatocellular carcinoma: biomarker discovery and therapeutic horizons.","authors":"Himanshi Goyal, Sachin Parwani, Jyotdeep Kaur","doi":"10.1038/s41420-024-02200-2","DOIUrl":"https://doi.org/10.1038/s41420-024-02200-2","url":null,"abstract":"Hepatocellular carcinoma (HCC) remains a significant global health challenge with few effective treatment options. The dysregulation of endoplasmic reticulum (ER) stress responses has emerged as a pivotal factor in HCC progression and therapy resistance. Long non-coding RNAs (lncRNAs) play a crucial role as key epigenetic modifiers in this process. Recent research has explored how lncRNAs influence ER stress which in turn affects lncRNAs activity in HCC. We systematically analyze the current literature to highlight the regulatory roles of lncRNAs in modulating ER stress and vice versa in HCC. Our scrutinization highlights how dysregulated lncRNAs contribute to various facets of HCC, including apoptosis resistance, enhanced proliferation, invasion, and metastasis, all driven by ER stress. Moreover, we delve into the emerging paradigm of the lncRNA-miRNA-mRNA axis, elucidating it as the promising avenue for developing novel biomarkers and paving the way for more personalized treatment options in HCC. Nevertheless, we acknowledge the challenges and future directions in translating these insights into clinical practice. In conclusion, our review provides insights into the complex regulatory mechanisms governing ER stress modulation by lncRNAs in HCC.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"10 1","pages":"451"},"PeriodicalIF":6.1,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11502918/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495899","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

Author Correction: Human adipose tissue-derived mesenchymal stem cells and their extracellular vesicles modulate lipopolysaccharide activated human microglia. 作者更正：人脂肪组织间充质干细胞及其细胞外囊泡可调节脂多糖激活的人小胶质细胞。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2024-10-23 DOI: 10.1038/s41420-024-02209-7

Marta Garcia-Contreras, Avnesh S Thakor

引用次数: 0