Apoptosis最新文献

{"title":"A deadly taste: linking bitter taste receptors and apoptosis","authors":"Zoey A. Miller,&nbsp;Ryan M. Carey,&nbsp;Robert J. Lee","doi":"10.1007/s10495-025-02091-3","DOIUrl":"10.1007/s10495-025-02091-3","url":null,"abstract":"<div><p>Humans can perceive five canonical tastes: salty, sour, umami, sweet, and bitter. These tastes are transmitted through the activation of ion channels and receptors. Bitter taste receptors (Taste Family 2 Receptors; T2Rs) are a sub-family of 25 G-protein coupled receptor (GPCR) isoforms that were first identified in type II taste bud cells. T2Rs are activated by a broad array of bitter agonists, which cause an increase in intracellular calcium (Ca²⁺) and a decrease in cyclic adenosine 3’,5’-monophosphate (cAMP). Interestingly, T2Rs are expressed beyond the oral cavity, where they play diverse non-taste roles in cell physiology and disease. Here, we summarize the literature that explores the role of T2Rs in apoptosis. Activation of T2Rs with bitter agonists induces apoptosis in several cancers, the airway epithelia, smooth muscle, and more. In many of these tissues, T2R activation causes mitochondrial Ca²⁺ overload, a main driver of apoptosis. This response may be a result of T2R cellular localization, nuclear Ca²⁺ mobilization and/or a remnant of the established immunological roles of T2Rs in other cell types. T2R-induced apoptosis could be pharmacologically leveraged to treat diseases of altered cellular proliferation. Future work must explore additional extra-oral T2R-expressing tissues for apoptotic responses, develop methods for <i>in-vivo</i> studies, and discover high affinity bitter agonists for clinical application.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 3-4","pages":"674 - 692"},"PeriodicalIF":6.1,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10495-025-02091-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143466725","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":"New insights into pulmonary arterial hypertension: interaction between PANoptosis and perivascular inflammatory responses.","authors":"Xianli Su, Yinhui Sun, Aiguo Dai","doi":"10.1007/s10495-025-02086-0","DOIUrl":"https://doi.org/10.1007/s10495-025-02086-0","url":null,"abstract":"<p><p>Pulmonary arterial hypertension (PAH) is a heterogeneous disease characterized by various etiologies, with pulmonary vascular remodeling recognized as a main pathological change. Currently, it is widely accepted that vascular remodeling is closely associated with abnormal pulmonary vascular cell death and perivascular inflammation. The simultaneous activation of various pulmonary vascular cell death leads to immune cell adhesion and inflammatory mediator releases; And in turn, the inflammatory response may also trigger cell death and jointly promote the progression of vascular remodeling. Recently, PANoptosis has been identified as a phenomenon that describes the simultaneous activation and interaction of multiple forms of programmed cell death (PCD). Therefore, the relationship between PANoptosis and inflammation in PAH warrants further investigation. This review examines the mechanisms underlying apoptosis, necroptosis, pyroptosis, and inflammatory responses in PAH, with a focus on PANoptosis and its interactions with inflammation. And it aims to elucidate the significance of this emerging form of cell death and inflammation in the pathophysiology of PAH and to explore its potential as a therapeutic target.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143466728","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}

{"title":"Integrating single-cell sequencing and machine learning to uncover the role of mitophagy in subtyping and prognosis of esophageal cancer","authors":"Feng Tian,&nbsp;Xinyang He,&nbsp;Saiwei Wang,&nbsp;Yiwei Liang,&nbsp;Zijie Wang,&nbsp;Minxuan Hu,&nbsp;Yaxian Gao","doi":"10.1007/s10495-024-02061-1","DOIUrl":"10.1007/s10495-024-02061-1","url":null,"abstract":"<div><p>Globally, esophageal cancer stands as a prominent contributor to cancer-related fatalities, distinguished by its poor prognosis. Mitophagy has a significant impact on the process of cancer progression. This study investigated the prognostic significance of mitophagy-related genes (MRGs) in esophageal carcinoma (ESCA) to elucidate molecular subtypes. By analyzing RNA-seq data from The Cancer Genome Atlas (TCGA), 6451 differentially expressed genes (DEGs) were identified. Cox regression analysis narrowed this list to 14 MRGs with potential prognostic implications. ESCA patients were classified into two distinct subtypes (C1 and C2) based on these genes. Furthermore, leveraging the differentially expressed genes between Cluster 1 and Cluster 2, ESCA patients were classified into two novel subtypes (CA and CB). Importantly, patients in C2 and CA subtypes exhibited inferior prognosis compared to those in C1 and CB (p &lt; 0.05). Functional enrichments and immune microenvironments varied significantly among these subtypes, with C1 and CB demonstrating higher immune checkpoint expression levels. Employing machine learning algorithms like LASSO regression, Random Forest and XGBoost, alongside multivariate COX regression analysis, two core genes: HSPD1 and MAP1LC3B were identified. A prognostic model based on these genes was developed and validated in two external cohorts. Additionally, single-cell sequencing analysis provided novel insights into esophageal cancer microenvironment heterogeneity. Through Coremine database screening, Icaritin emerged as a potential therapeutic candidate to potentially improve esophageal cancer prognosis. Molecular docking results indicated favorable binding efficacies of Icaritin with HSPD1 and MAP1LC3B, contributing to the understanding of the underlying molecular mechanisms of esophageal cancer and offering therapeutic avenues.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 3-4","pages":"1021 - 1041"},"PeriodicalIF":6.1,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413067","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}

{"title":"The complexities of cell death mechanisms: a new perspective in systemic sclerosis therapy","authors":"Xue Xia,&nbsp;Chenfei Kong,&nbsp;Xiaoming Zhao,&nbsp;Kelin Zhao,&nbsp;Naixu Shi,&nbsp;Jinlan Jiang,&nbsp;Ping Li","doi":"10.1007/s10495-025-02082-4","DOIUrl":"10.1007/s10495-025-02082-4","url":null,"abstract":"<div><p>Systemic sclerosis, also termed scleroderma, is a severe and debilitating autoimmune disease characterized by fibrosis, an aberrant immune response, and vascular dysfunction. Cell death is essential to the body’s continued normal development as it removes old or damaged cells. This process is governed by several mechanisms, including programmed cell death through apoptosis, necrosis, and pyroptosis, as well as metabolic processes, such as ferroptosis and cuproptosis. This review describes the signaling pathways associated with each form of cell death, examining the linkages between these pathways, and discussing how the dysregulation of cell death processes is involved in the development of autoimmune disorders such as systemic sclerosis. Existing and promising therapeutic strategies aimed at restoring the balance of cell death in systemic sclerosis and other autoimmune disorders are also emphasized.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 3-4","pages":"636 - 651"},"PeriodicalIF":6.1,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381632","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}

{"title":"Effects of microplastics on chemo-resistance and tumorigenesis of colorectal cancer","authors":"Wen Pan,&nbsp;Yueting Han,&nbsp;Mingqing Zhang,&nbsp;Kegan Zhu,&nbsp;Zhen Yang,&nbsp;Minghan Qiu,&nbsp;Yaoyang Guo,&nbsp;Ziyi Dong,&nbsp;Jie Hao,&nbsp;Xipeng Zhang,&nbsp;Ming Gao,&nbsp;Haiyang Zhang","doi":"10.1007/s10495-025-02085-1","DOIUrl":"10.1007/s10495-025-02085-1","url":null,"abstract":"<div><p>Microplastics (MPs) are widely distributed environmental pollutants around the world. Although studies have demonstrated that MPs have adverse effects on human health, the relationship between MPs and tumors remains unclear. The gut is the main site of microplastics absorption, and the function of MPs in the chemoresistance and progression of colorectal cancer (CRC) needs more investigation. Here, we show that MPs exist in human CRC tissues for the first time by using a laser direct infrared chemical imaging system. MPs can cause an increase in CRC incidence in animal models and promote resistance to oxaliplatin. It is illustrated that the uptake of MPs enhances levels of autophagy by activating the mTOR pathway. MPs can also promote the disorder of intestinal flora and intestinal inflammation, serving as an essential component in the onset and advancement of CRC. These results indicated that microplastic pollutants in colorectal cancer could mediate protective autophagy through the mTOR/ULK1 axis, which is one of the new reasons for chemo-resistance in CRC under the background of increasingly serious microplastics pollution. This study identified the adverse effects of MPs on colorectal cancer progression and chemotherapy prognosis, and attempted to block the intake of MPs to propose a novel approach for clinical precision treatment.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 3-4","pages":"1005 - 1020"},"PeriodicalIF":6.1,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381616","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}

{"title":"A cellular danse macabre: the choreography of programmed cell death","authors":"Arjan W. Griffioen,&nbsp;Patrycja Nowak-Sliwinska","doi":"10.1007/s10495-025-02076-2","DOIUrl":"10.1007/s10495-025-02076-2","url":null,"abstract":"<div><p>Research on cell death is getting diverse. Apoptosis and other forms of programmed cell death play a critical role in maintaining cellular homeostasis and defending an organism from infections, cancer, and degenerative diseases. Apoptosis, a well-known form of programmed cell death, involves non-inflammatory and orderly organized dismantling of a cell. Different pathways and mechanisms have emerged that challenge the traditional apoptosis-centric view, such as necroptosis, panoptosis, pyroptosis, paraptosis, ferroptosis and autophagic cell death. This editorial aims to highlight some of these emerging pathways, expanding our understanding of cellular death and its implications in health and disease. Over the years, <i>Apoptosis</i> has been at the forefront of publishing discoveries on these diverse and impactful processes.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 3-4","pages":"507 - 511"},"PeriodicalIF":6.1,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381611","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}

{"title":"Itaconate promotes mitophagy to inhibit neuronal ferroptosis after subarachnoid hemorrhage","authors":"Guijun Wang,&nbsp;Zhijie Li,&nbsp;Wenrui Han,&nbsp;Qi Tian,&nbsp;Chengli Liu,&nbsp;Shengming Jiang,&nbsp;Xi Xiang,&nbsp;Xincan Zhao,&nbsp;Lei Wang,&nbsp;Jianming Liao,&nbsp;Mingchang Li","doi":"10.1007/s10495-025-02077-1","DOIUrl":"10.1007/s10495-025-02077-1","url":null,"abstract":"<div><p>Subarachnoid hemorrhage (SAH), representing 5–10% of all stroke cases, is a cerebrovascular event associated with a high mortality rate and a challenging prognosis. The role of IRG1-regulated itaconate in bridging metabolism, inflammation, oxidative stress, and immune response is pivotal; however, its implications in the early brain injury following SAH remain elusive. The SAH nerve inflammation model was constructed by Hemin solution and BV2 cells. In vitro and in vivo SAH models were established by intravascular puncture and Hemin solution treatment of HT22 cells. To explore the relationship between IRG1 and neuroinflammation by interfering the expression of Irg1 in BV2 cells. By adding itaconate and its derivatives to explore the relationship between mitophagy and ferroptosis. IRG1 knockdown increased the expression of inflammatory factors and induced the transformation of microglia to pro-inflammatory phenotype after SAH; Itaconate and itaconate derivative 4-OI can reduce oxidative stress and lipid peroxidation level in neuron after SAH, and reduce EBI after SAH; IRG1/ itaconate promotes mitophagy through PINK1/Parkin signaling pathway to inhibit neuronal ferroptosis. IRG1 can improve nerve inflammation after SAH, M2 of microglia induced polarization. IRG1/ Itaconate participates in mitophagy through PINK1/Parkin to alleviate neuronal ferroptosis after SAH and play a neuroprotective role.</p><h3>Graphical Abstract</h3><div><figure><div><div><picture><source><img></source></picture></div><div><p>Resting microglia are exposed to external stimuli, a subset of them will undergo polarization to the M2 phenotype. Within M2 microglia, the enzyme IRG1/ACOD1 facilitates the conversion of cis-aconitate to itaconate in the tricarboxylic acid cycle, which is subsequently secreted into the extracellular space. This itaconic acid is taken up by neurons and promotes mitochondrial autophagy, ultimately reducing oxidative stress and inhibiting neuronal ferroptosis. This graphic was created using the painting tool on the Biorender website. (Picture is drawn using biorender)</p></div></div></figure></div></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 3-4","pages":"991 - 1004"},"PeriodicalIF":6.1,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381630","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}

{"title":"Cell death signaling in human erythron: erythrocytes lose the complexity of cell death machinery upon maturation","authors":"Anton Tkachenko,&nbsp;Ondrej Havranek","doi":"10.1007/s10495-025-02081-5","DOIUrl":"10.1007/s10495-025-02081-5","url":null,"abstract":"<div><p>Over the recent years, our understanding of the cell death machinery of mature erythrocytes has been greatly expanded. It resulted in the discovery of several regulated cell death (RCD) pathways in red blood cells. Apoptosis (eryptosis) and necroptosis of erythrocytes share certain features with their counterparts in nucleated cells, but they are also critically different in particular details. In this review article, we summarize the cell death subroutines in the erythroid precursors (apoptosis, necroptosis, and ferroptosis) in comparison to mature erythrocytes (eryptosis and erythronecroptosis) to highlight the consequences of organelle clearance and associated loss of multiple components of the cell death machinery upon erythrocyte maturation. Recent advances in understanding the role of erythrocyte RCDs in health and disease have expanded potential clinical applications of these lethal subroutines, emphasizing their contribution to the development of anemia, microthrombosis, and endothelial dysfunction, as well as their role as diagnostic biomarkers and markers of erythrocyte storage-induced lesions. Fas signaling and the functional caspase-8/caspase-3 system are not indispensable for eryptosis, but might be retained in mature erythrocytes to mediate the crosstalk between both erythrocyte-associated RCDs. The ability of erythrocytes to switch between eryptosis and necroptosis suggests that their cell death is not a simple unregulated mechanical disintegration, but a tightly controlled process. This allows investigation of eventual pharmacological interventions aimed at individual cell death subroutines of erythrocytes.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 3-4","pages":"652 - 673"},"PeriodicalIF":6.1,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10495-025-02081-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381614","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":"The impact of SEC23A on 5-FU chemotherapy sensitivity and its involvement in endoplasmic reticulum stress-induced apoptosis in colorectal cancer","authors":"Zhaoran Su,&nbsp;Menglan Liu,&nbsp;Mathias Krohn,&nbsp;Sandra Schwarz,&nbsp;Michael Linnebacher","doi":"10.1007/s10495-025-02084-2","DOIUrl":"10.1007/s10495-025-02084-2","url":null,"abstract":"<div><p>Background: Colorectal cancer (CRC) represents a significant global health burden, with chemotherapy resistance representing a significant challenge to effective treatment. SEC23A, a core component of the COPII vesicle trafficking system, is of critical importance with regard to protein transport and cellular homeostasis. Nevertheless, its function in CRC progression and chemoresistance remains uncertain. The present study investigates the correlation between SEC23A expression and sensitivity to 5-fluorouracil (5-FU), a widely used chemotherapeutic agent, with particular emphasis on ER stress-induced apoptosis. Methods: A bioinformatic analysis was conducted to evaluate SEC23A expression in CRC and its association with patient prognosis. Chemotherapy sensitivity was predicted using GDSC data and validated experimentally using CRC cell lines with manipulated SEC23A expression. In order to explore the role of SEC23A in acquired drug resistance, patient-derived xenograft (PDX) models and 5-FU-resistant cell lines were employed. Apoptosis assays, cell cycle analysis, and ER stress modulation experiments were performed to elucidate the underlying mechanisms. Results: SEC23A expression was significantly reduced in CRC samples compared to normal tissues. This reduction was linked to a poorer prognosis, including both overall and disease-specific survival. A correlation was observed between low SEC23A expression and increased resistance to 5-FU, as evidenced by both bioinformatic predictions and in vitro experiments. In PDX models, metastatic lesions exhibited decreased SEC23A expression following 5-FU treatment in comparison to primary tumors. Overexpression of SEC23A in 5-FU-resistant cell lines restored sensitivity to the drug and increased apoptosis. Bioinformatic and experimental analyses revealed a robust correlation between SEC23A and ER stress-related apoptotic pathways. Elevated expression of SEC23A was observed to facilitate the accumulation of misfolded proteins in response to 5-FU treatment, which in turn resulted in increased ER stress and apoptosis. Conclusions: SEC23A plays a crucial role in modulating the sensitivity of CRC cells to 5-FU by regulating ER stress-induced apoptosis. Its downregulation contributes to chemoresistance, indicating that SEC23A may serve as a prognostic marker and therapeutic target in CRC. Strategies aimed at upregulating SEC23A or enhancing ER stress may provide new avenues for overcoming chemoresistance and improving treatment outcomes for CRC patients.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 3-4","pages":"976 - 990"},"PeriodicalIF":6.1,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10495-025-02084-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188161","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":"Machine learning-based integration reveals immunological heterogeneity and the clinical potential of T cell receptor (TCR) gene pattern in hepatocellular carcinoma","authors":"Zewei Zhuo,&nbsp;Huihuan Wu,&nbsp;Lingli Xu,&nbsp;Yuran Ji,&nbsp;Jiezhuang Li,&nbsp;Liehui Liu,&nbsp;Hong Zhang,&nbsp;Qi Yang,&nbsp;Zhongwen Zheng,&nbsp;Weijian Lun","doi":"10.1007/s10495-025-02080-6","DOIUrl":"10.1007/s10495-025-02080-6","url":null,"abstract":"<div><p>The T Cell Receptor (TCR) significantly contributes to tumor immunity, whereas the intricate interplay with the Hepatocellular Carcinoma (HCC) microenvironment and clinical significance remains largely unexplored. Here, we aimed to examine the function of TCR signaling in tumor immunity and its clinical significance in HCC. Our objective was to employ TCR signaling genes and a machine learning-based integrative methodology to construct a prognostic prediction system termed the TCR score. Herein, we revealed that the TCR score serves as an independent risk factor for overall survival in HCC patients, demonstrating stable and robust performance. The accuracy of the TCR score significantly exceeds that of traditional clinical variables and published signatures. Additionally, the immune infiltration was abundant in patients with low TCR scores. Single-cell cohort analysis further demonstrates that patients with low TCR scores possess an immune-active tumor microenvironment (TME), with T/NK cells enhancing interactions with myeloid cells through signaling networks such as MIF, MK, and SPP1. In response to these changes in the TME, patients with high TCR scores exhibit poorer outcomes and shorter survival in immunotherapy cohorts. In vitro experiments demonstrated that the key TCR signaling biomarker SOS1 knockdown significantly suppresses the HCC cells’ capability to proliferate, invade, and migrate while enhancing tumor cell apoptosis. The TCR score could function as a robust and potential tool to predict immune activity and improve clinical outcomes for HCC patients.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 3-4","pages":"955 - 975"},"PeriodicalIF":6.1,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188147","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}