Cell Death Discovery最新文献

{"title":"CeDaD-a novel assay for simultaneous tracking of cell death and division in a single population.","authors":"Lukas Nöltner, Kurt Engeland, Robin Kohler","doi":"10.1038/s41420-025-02370-7","DOIUrl":"10.1038/s41420-025-02370-7","url":null,"abstract":"<p><p>The cell division cycle and the various forms of programmed cell death are interconnected. A prominent example is the tumor suppressor p53, which not only induces apoptosis but also plays an important role in the arrest of the cell cycle. Consequently, simultaneous analysis of cell division and cell death is frequently of significant interest in cell biology research. Traditionally, these processes require distinct assays, making concurrent analysis challenging. To address this, we present a novel combined assay, called CeDaD assay-Cell Death and Division assay-which allows for the simultaneous quantification of cell division and cell death within a single-cell population. This assay utilizes a straightforward flow cytometric approach, combining a staining based on carboxyfluorescein succinimidyl ester (CFSE) to monitor cell division with an annexin V-derived staining to assess the extent of cell death.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"86"},"PeriodicalIF":6.1,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11880512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143556008","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}

{"title":"Capsanthin inhibits migration and reduces N-linked glycosylation of PD-L1 via the EZH2-PD-L1 axis in triple-negative breast cancer brain metastasis.","authors":"Yi-Chung Chien, Jia-Yan Wu, Liang-Chih Liu, Yung-Luen Yu","doi":"10.1038/s41420-025-02368-1","DOIUrl":"10.1038/s41420-025-02368-1","url":null,"abstract":"<p><p>Breast cancer metastasis to the brain, occurring in about 15-25% of cases, represents a major obstacle in the treatment of triple-negative breast cancer (TNBC). The molecular mechanisms driving this form of metastasis are still largely unknown. PD-L1, an immune checkpoint protein, is central to tumor immune evasion and has become a focus for immunotherapy development. While PD-L1 inhibitors have shown success in various cancer types, their effectiveness in TNBC brain metastases remains to be fully investigated. This highlights the urgent need to understand the complex interactions between metastatic brain tumors and the tumor microenvironment in TNBC patients. Gaining insights into these dynamics is crucial for developing new targeted therapies, including those that modulate the PD-L1 pathway, to better manage and treat TNBC brain metastases. We explore the impact of Capsanthin on the tumor microenvironment of brain metastases in triple-negative breast cancer (TNBC). Our results reveal that Capsanthin effectively inhibits the migration of brain metastasis TNBC cells. Furthermore, Capsanthin significantly reduces the expression of EZH2 and N-linked glycosylated PD-L1 proteins and mRNA in TNBC cells, encompassing both primary and metastatic sites, as well as in mesenchymal stem cells (3A6). Data from The Cancer Genome Atlas (TCGA) indicate that elevated expression levels of EZH2 correlate with poorer patient prognosis. Immunoprecipitation assays demonstrate a direct interaction between EZH2 and PD-L1 in brain metastases of TNBC, underscoring the pivotal role of the EZH2-PD-L1 axis. Additionally, Capsanthin was found to suppress the expression of epithelial-mesenchymal transition (EMT) markers in metastatic brain TNBC cells and mesenchymal stem cells. Our results suggest that Capsanthin can modulate the tumor microenvironment and inhibit key pathways involved in cancer progression, offering potential therapeutic benefits for patients with TNBC brain metastases.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"85"},"PeriodicalIF":6.1,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11880297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555956","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}

{"title":"Enhancer reprogramming: critical roles in cancer and promising therapeutic strategies.","authors":"Jinshou Yang, Feihan Zhou, Xiyuan Luo, Yuan Fang, Xing Wang, Xiaohong Liu, Ruiling Xiao, Decheng Jiang, Yuemeng Tang, Gang Yang, Lei You, Yupei Zhao","doi":"10.1038/s41420-025-02366-3","DOIUrl":"10.1038/s41420-025-02366-3","url":null,"abstract":"<p><p>Transcriptional dysregulation is a hallmark of cancer initiation and progression, driven by genetic and epigenetic alterations. Enhancer reprogramming has emerged as a pivotal driver of carcinogenesis, with cancer cells often relying on aberrant transcriptional programs. The advent of high-throughput sequencing technologies has provided critical insights into enhancer reprogramming events and their role in malignancy. While targeting enhancers presents a promising therapeutic strategy, significant challenges remain. These include the off-target effects of enhancer-targeting technologies, the complexity and redundancy of enhancer networks, and the dynamic nature of enhancer reprogramming, which may contribute to therapeutic resistance. This review comprehensively encapsulates the structural attributes of enhancers, delineates the mechanisms underlying their dysregulation in malignant transformation, and evaluates the therapeutic opportunities and limitations associated with targeting enhancers in cancer.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"84"},"PeriodicalIF":6.1,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11876437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540278","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}

{"title":"Insufficient expression of COL6A1 promotes the development of early-onset severe preeclampsia by inhibiting the APJ/AKT signaling pathway.","authors":"Gonghua Qi, Yanmin Gong, Yi Li, Yanhui Jin, Shuqi Chi, Wenxia Zhang, Xia Luo","doi":"10.1038/s41420-025-02373-4","DOIUrl":"10.1038/s41420-025-02373-4","url":null,"abstract":"<p><p>Early-onset severe preeclampsia (eosPE) is one of the most severe complications of pregnancy. To identify the genes related to the development of eosPE. We downloaded and integrated analyzed microarray data from GSE44711, GSE66273, and GSE74341, which contains the expression profile of placental tissues from patients with eosPE and healthy controls. Our analysis revealed that collagen type VI alpha 1 (COL6A1) was downregulated in the eosPE placenta compared to normal pregnancy. COL6A1 promoted the migration, invasion and tube formation ability of HTR8/SVneo cells, HUVECs and primary extravillous trophoblasts (EVTs). To explore the underlying mechanisms, we conducted transcriptome sequencing, which indicated that the Apelin/APJ signaling pathway was affected by COL6A1 knockdown. In addition, we found that APJ expression was lower in the placental tissue of patients with eosPE compared to healthy pregnancies. Inhibition of APJ suppressed the invasion, migration, and tube formation abilities of trophoblasts. We also observed that COL6A1 increased the levels of p-AKT and p-mTOR, while the APJ inhibitor ML221 impaired this effect. Furthermore, transwell and tube formation assays demonstrated that ML221 attenuated the capabilities enhanced by COL6A1, an effect that could be rescued by the AKT activator SC79. Overall, these findings indicate that insufficient expression of COL6A1 attenuates the migration, invasion, and endothelial-like tube formation of HTR8/SVneo cells and primary EVTs via the APJ/AKT/mTOR pathway, thereby promoting the development of eosPE.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"81"},"PeriodicalIF":6.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11873267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536676","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}

{"title":"Discoidin domain receptor inhibitor DDR1-IN-1 induces autophagy and necroptotic cell death in malignant peripheral nerve sheath tumor.","authors":"Guan-Yi Lai, Yu-Cheng Lee, Hao-Jui Weng, Kuei-Hung Lai, Min-Chen Hsiang, Kai-Yu Hsu, Chung-Ping Liao","doi":"10.1038/s41420-025-02367-2","DOIUrl":"10.1038/s41420-025-02367-2","url":null,"abstract":"<p><p>Malignant peripheral nerve sheath tumor (MPNST) is a soft tissue sarcoma commonly associated with the tumor-predisposition disorder neurofibromatosis 1. The extracellular matrix collagens contribute to many fibrotic tumors; however, the role of collagen signaling in MPNST was unclear. This study investigated the effects of blocking the interaction between collagens and their receptors in MPNST. We first analyzed the expressions of collagen family proteins in MPNSTs and found an overall increase compared to neurofibroma. Treatment of DDR1-IN-1, a small molecule inhibitor for the collagen receptor discoidin domain receptor, induced a robust MPNST cell death, highlighting the dependence of MPNST survival on collagen signaling. DDR1-IN-1 induced MPNST cell death by activating autophagy and necroptosis signaling. Treatment of necroptosis inhibitors necrostatin-1 or necrosulfonamide reduced the numbers of DDR1-IN-1-induced necrotic cells and autolysosomes, suggesting that the autophagic process depends on necroptosis activation. Combinations of DDR1-IN-1 with other anti-MPNST agents revealed synergistic activities against MPNST. In summary, this study discovered a critical MPNST death signaling induced by the small molecule DDR1-IN-1, which might shed light on future MPNST therapeutic strategies.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"83"},"PeriodicalIF":6.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11873111/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536617","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}

{"title":"NDUFB7 mutations cause brain neuronal defects, lactic acidosis, and mitochondrial dysfunction in humans and zebrafish.","authors":"Yen-Lin Chen, Brian Hon-Yin Chung, Masakazu Mimaki, Shumpei Uchino, Yin-Hsiu Chien, Christopher Chun-Yun Mak, Steven Shinn-Forng Peng, Wei-Chen Wang, Yu-Li Lin, Wuh-Liang Hwu, Shyh-Jye Lee, Ni-Chung Lee","doi":"10.1038/s41420-025-02369-0","DOIUrl":"10.1038/s41420-025-02369-0","url":null,"abstract":"<p><p>Complex I of the mitochondrial electron transfer chain is one of the largest membrane protein assemblies ever discovered. A patient carrying a homozygous NDUFB7 intronic mutation died within two months after birth due to cardiorespiratory defects, preventing further study. Here, we report another patient with compound heterozygous mutations in NDUFB7 who suffers from pons abnormality, lactic acidosis, prematurity, prenatal and postnatal growth deficiency, incomplete closure of the abdominal wall (ventral hernia), and a poorly functioning gastrointestinal tract (pseudo-obstruction). We demonstrated that the patient's skin fibroblasts are deficient in Complex I assembly and reduced supercomplex formation. This report further broadens the spectrum of mitochondrial disorders. The patient has had several surgeries. After receiving treatment with Coenzyme Q10 and vitamin B complex, she has remained stable up to this point. To further explore the functionality of NDUFB7 in vivo, we knocked down Ndufb7 in zebrafish embryos. This resulted in brain ventricle and neuronal defects, elevated lactic acid levels, and reduced oxygen consumption, indicating defective mitochondrial respiration. These phenotypes can be specifically rescued by ectopic expression of ndufb7. More importantly, Mitoquinone mesylate (MitoQ), a common remedy for mitochondrial disorders, can ameliorate these conditions. These results suggest a role for NDUFB7 in mitochondrial activity and the suitability of the zebrafish model for further drug screening and the development of therapeutic strategies for this rare disease.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"82"},"PeriodicalIF":6.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11873233/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536682","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}

{"title":"Loss of TC-PTP in keratinocytes leads to increased UVB-induced autophagy.","authors":"Obed Asare, Lindsey Shim, Cheol-Jung Lee, Jose Delgado, Natasha Quailes, Klarissa Zavala, Junsoo Park, Bilal Bin Hafeez, Yong-Yeon Cho, Subhash C Chauhan, Dae Joon Kim","doi":"10.1038/s41420-025-02353-8","DOIUrl":"10.1038/s41420-025-02353-8","url":null,"abstract":"<p><p>Ultraviolet B (UVB) radiation can distort cellular homeostasis and predispose the skin to carcinogenesis. Amongst the deteriorating effects of the sun's UVB radiation on cellular homeostasis is the formation of DNA photoproducts. These photoproducts can cause significant changes in the structure and conformation of DNA, inducing gene mutations which may accumulate to trigger the formation of skin cancer. Photoproducts are typically repaired by nucleotide excision repair. Notwithstanding, when the repair mechanism fails, apoptosis ensues to prevent the accumulation of mutations and to restore cellular homeostasis. This present study reports that T-cell protein tyrosine phosphatase (TC-PTP) can increase UVB-induced apoptosis by inhibiting autophagy-mediated cell survival of damaged keratinocytes. TC-PTP deficiency in 3PC mouse keratinocytes led to the formation of autophagic vacuoles and increased expression of LC3-II. We established human TC-PTP-deficient (TC-PTP/KO) HaCaT cells using the CRISPR/Cas9 system. TC-PTP/KO HaCaT cells exhibited increased cell survival upon UVB exposure, which was accompanied by increased expression of LC3-II and decreased expression of p62 compared to control cells. Pretreatment of TC-PTP/KO HaCaT cells with early-phase autophagy inhibitor, 3-methyladenine significantly decreased the expression of LC3-II and reduced cell survival in response to UVB irradiation in comparison with untreated TC-PTP/KO cells. Pretreatment of TC-PTP/KO HaCaT cells with late-phase inhibitor, chloroquine also significantly reduced cell viability with increased accumulation of LC3-II after UVB irradiation compared to untreated counterpart cells. While UVB significantly increased apoptosis in the engineered (Mock) cells, this was not observed in similarly treated TC-PTP/KO HaCaT cells. However, chloroquine treatment increased apoptosis in TC-PTP/KO HaCaT cells. Examination of human squamous cell carcinomas (SCCs) revealed that TC-PTP expression was inversely correlated with LC3 expression. Our findings suggest that TC-PTP negatively regulates autophagy-mediated survival of damaged cells following UVB exposure, which can contribute to remove damaged keratinocytes via apoptosis.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"80"},"PeriodicalIF":6.1,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11871011/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531337","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}

{"title":"Insights from lipidomics into the terminal maturation of circulating human reticulocytes.","authors":"Giampaolo Minetti, Isabel Dorn, Harald Köfeler, Cesare Perotti, Lars Kaestner","doi":"10.1038/s41420-025-02318-x","DOIUrl":"10.1038/s41420-025-02318-x","url":null,"abstract":"<p><p>In the age of \"omics\", lipidomics of erythropoiesis is still missing. How reticulocytes mature in the circulation into functional erythrocytes is also largely unknown. We have isolated here two populations of human circulating reticulocytes at different levels of maturation, and three subpopulations of erythrocytes of different age, and characterized the evolution of their lipidome. (Sphingomyelin+cholesterol) and partly phosphatidylethanolamine increase relative to total lipids, whereas phosphatidylcholine and phosphatidylserine decrease from immature reticulocytes to mature erythrocytes, at the same time as the surface area per cell decreases. The relative amounts of more than 70 phospholipid subclasses, based on the number of carbon atoms (12-24) and of double bonds (0-6) in the fatty acids linked to the phospholipid, also change in the process. As reticulocytes and erythrocytes cannot perform de-novo phospholipid synthesis, lipid remodeling likely requires selective removal of phospholipids from the membrane or their exchange with plasma or both, with the possible involvement of lipid transfer proteins such as VPS13A, which is expressed in reticulocytes and erythrocytes. These findings not only shed light on fundamental aspects of red blood cell physiology and erythropoiesis but also raise intriguing questions surrounding protein-lipid interactions, membrane architecture, and lipid trafficking mechanisms.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"79"},"PeriodicalIF":6.1,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11868425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522696","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}

{"title":"Crosstalk between gut microbiotas and fatty acid metabolism in colorectal cancer.","authors":"Hao Zhang, Yuan Tian, Chunjie Xu, Miaomiao Chen, Zeyu Xiang, Lei Gu, Hanbing Xue, Qing Xu","doi":"10.1038/s41420-025-02364-5","DOIUrl":"10.1038/s41420-025-02364-5","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is the third most common malignancy globally and the second leading cause of cancer-related mortality. Its development is a multifactorial and multistage process influenced by a dynamic interplay between gut microbiota, environmental factors, and fatty acid metabolism. Dysbiosis of intestinal microbiota and abnormalities in microbiota-associated metabolites have been implicated in colorectal carcinogenesis, highlighting the pivotal role of microbial and metabolic interactions. Fatty acid metabolism serves as a critical nexus linking dietary patterns with gut microbial activity, significantly impacting intestinal health. In CRC patients, reduced levels of short-chain fatty acids (SCFAs) and SCFA-producing bacteria have been consistently observed. Supplementation with SCFA-producing probiotics has demonstrated tumor-suppressive effects, while therapeutic strategies aimed at modulating SCFA levels have shown potential in enhancing the efficacy of radiation therapy and immunotherapy in both preclinical and clinical settings. This review explores the intricate relationship between gut microbiota, fatty acid metabolism, and CRC, offering insights into the underlying mechanisms and their potential translational applications. Understanding this interplay could pave the way for novel diagnostic, therapeutic, and preventive strategies in the management of CRC.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"78"},"PeriodicalIF":6.1,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11865559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514804","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}

{"title":"NFIX suppresses breast cancer cell proliferation by delaying mitosis through downregulation of CDK1 expression.","authors":"Hai-Yan Ma, Rui Sun, Tian Tian, Xue-Jie Zhou, Zhao-Hui Chen, Xu-Chen Cao, Yue Yu, Xin Wang","doi":"10.1038/s41420-025-02361-8","DOIUrl":"10.1038/s41420-025-02361-8","url":null,"abstract":"<p><p>One of the fundamental biological characteristics of malignant tumors is their uncontrolled growth and multiplication, which is a major reason why breast cancer remains incurable. The significance of NFIX in the development of various cancers has been demonstrated by an increasing number of studies in recent years. However, the role of NFIX in breast cancer has received less attention. This study investigates its expression in breast cancer and its function in inhibiting cell cycle progression. NFIX is downregulated in breast cancer compared to normal breast tissue, which impacts prognosis. In vitro and in vivo Experiments have shown that the overexpression of NIFX leads to a delay in the G2/M phase, which inhibits breast cancer cell proliferation. It thus plays a role as a tumor suppressor in breast cancer development. In terms of mechanism, upregulating NFIX causes CDK1 to be more susceptible to ubiquitination-mediated degradation. NFIX also competitively represses CDK1 transcription via YBX1. Moreover, NFIX expression in breast cancer is associated with methylation of its promoter region. Our study demonstrated that NFIX plays a critical role in CDK1-regulated cell cycle transitions and determined that NFIX inhibits cell proliferation in breast cancer.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"77"},"PeriodicalIF":6.1,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11861311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143499163","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}