Apoptosis最新文献

{"title":"LIPUS regulates the progression of knee osteoarthritis in mice through primary cilia-mediated TRPV4 channels","authors":"Sha Wu,&nbsp;Haiqi Zhou,&nbsp;Huixian Ling,&nbsp;Yuyan Sun,&nbsp;Ziyu Luo,&nbsp;ThaiNamanh Ngo,&nbsp;Yuanyuan Fu,&nbsp;Wen Wang,&nbsp;Ying Kong","doi":"10.1007/s10495-024-01950-9","DOIUrl":"10.1007/s10495-024-01950-9","url":null,"abstract":"<div><p>Osteoarthritis (OA) is a common disease in middle-aged and elderly people. An imbalance in calcium ion homeostasis will contribute to chondrocyte apoptosis and ultimately lead to the progression of OA. Transient receptor potential channel 4 (TRPV4) is involved in the regulation of intracellular calcium homeostasis. TRPV4 is expressed in primary cilia, which can sense mechanical stimuli from outside the cell, and its abnormal expression is closely related to the development of OA. Low-intensity pulsed ultrasound (LIPUS) can alleviate chondrocyte apoptosis while the exact mechanism is unclear. In this project, with the aim of revealing the mechanism of action of LIPUS, we proposed to use OA chondrocytes and animal models, LIPUS intervention, inhibition of primary cilia, use TRPV4 inhibitors or TRPV4 agonist, and use Immunofluorescence (IF), Immunohistochemistry (IHC), Western Blot (WB), Quantitative Real-time PCR (QP) to detect the expression of cartilage synthetic matrix and endoplasmic reticulum stress markers. The results revealed that LIPUS altered primary cilia expression, promoted synthetic matrix metabolism in articular chondrocytes and was associated with primary cilia. In addition, LIPUS exerted a active effect on OA by activating TRPV4, inducing calcium inward flow, and facilitating the entry of NF-κB into the nucleus to regulate synthetic matrix gene transcription. Inhibition of TRPV4 altered primary cilia expression in response to LIPUS stimulation, and knockdown of primary cilia similarly inhibited TRPV4 function. These results suggest that LIPUS mediates TRPV4 channels through primary cilia to regulate the process of knee osteoarthritis in mice.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 5-6","pages":"785 - 798"},"PeriodicalIF":6.1,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11055729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140189403","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":"Novel CAR-T cells targeting TRKB for the treatment of solid cancer","authors":"Dandan Liang,&nbsp;Jie Tang,&nbsp;Bin Sun,&nbsp;Shuai He,&nbsp;Dong Yang,&nbsp;Haiyan Ma,&nbsp;Yuncang Yun,&nbsp;Yongjie Zhu,&nbsp;Wenwen Wei,&nbsp;Haiyang Chen,&nbsp;Xudong Zhao","doi":"10.1007/s10495-024-01936-7","DOIUrl":"10.1007/s10495-024-01936-7","url":null,"abstract":"<div><p>Chimeric antigen receptor (CAR) T-cell therapy is highly effective for treating blood cancers such as B-cell malignancies, however, its effectiveness as an approach to treat solid tumors remains to be further explored. Here, we focused on the development of CAR-T cell therapies targeting tropomyosin-related kinase receptor B (TRKB), a highly expressed protein that is significantly associated with tumor progression, malignancy, and drug resistance in multiple forms of aggressive solid tumors. To achieve this, we screened brain-derived neurotrophic factor (BDNF) and neurotrophin 4 (NTF4) ligand-based CAR-T cells for their efficiency in targeting the TRKB receptor in the context of solid tumors, particularly hepatocellular carcinoma and pancreatic cancer. We demonstrated that TRKB is overexpressed not only in hepatocellular carcinoma and pancreatic carcinoma cell lines but also in cancer stem-like cells (CSCs). Notably, BDNF-CAR T and NTF4-CAR T cells could not only effectively target and kill TRKB-expressing pan-cancer cell lines in a dose-dependent manner but also effectively kill CSCs. We also performed in vivo studies to show that NTF4-CAR T cells have a better potential to inhibit the tumor growth of hepatocellular carcinoma xenografts in mice, compared with BDNF-CAR T cells. Taken together, our findings suggest that CAR-T targeting TRKB may be a promising approach for developing novel therapies to treat solid cancers.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 11-12","pages":"2183 - 2196"},"PeriodicalIF":6.1,"publicationDate":"2024-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140157439","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 novel mitochondrial unfolded protein response-related risk signature to predict prognosis, immunotherapy and sorafenib sensitivity in hepatocellular carcinoma","authors":"Sidi Zhang,&nbsp;Hanyao Guo,&nbsp;Hongyu Wang,&nbsp;Xiaopeng Liu,&nbsp;Meixia Wang,&nbsp;Xiaoyu Liu,&nbsp;Yumei Fan,&nbsp;Ke Tan","doi":"10.1007/s10495-024-01945-6","DOIUrl":"10.1007/s10495-024-01945-6","url":null,"abstract":"<div><p>Hepatocellular carcinoma (HCC) is a common cause of cancer-associated death worldwide. The mitochondrial unfolded protein response (UPR^mt) not only maintains mitochondrial integrity but also regulates cancer progression and drug resistance. However, no study has used the UPR^mt to construct a prognostic signature for HCC. This work aimed to establish a novel signature for predicting patient prognosis, immune cell infiltration, immunotherapy, and chemotherapy response based on UPR^mt-related genes (MRGs). Transcriptional profiles and clinical information were obtained from the TCGA and ICGC databases. Cox regression and LASSO regression analyses were applied to select prognostic genes and develop a risk model. The TIMER algorithm was used to investigate immunocytic infiltration in the high- and low-risk subgroups. Here, two distinct clusters were identified with different prognoses, immune cell infiltration statuses, drug sensitivities, and response to immunotherapy. A risk score consisting of seven MRGs (HSPD1, LONP1, SSBP1, MRPS5, YME1L1, HDAC1 and HDAC2) was developed to accurately and independently predict the prognosis of HCC patients. Additionally, the expression of core MRGs was confirmed by immunohistochemistry (IHC) staining, single-cell RNA sequencing, and spatial transcriptome analyses. Notably, the expression of prognostic MRGs was significantly correlated with sorafenib sensitivity in HCC and markedly downregulated in sorafenib-treated HepG2 and Huh7 cells. Furthermore, the knockdown of LONP1 decreased the proliferation, invasion, and migration of HepG2 cells, suggesting that upregulated LONP1 expression contributed to the malignant behaviors of HCC cells. To our knowledge, this is the first study to investigate the consensus clustering algorithm, prognostic potential, immune microenvironment infiltration and drug sensitivity based on the expression of MRGs in HCC. In summary, the UPR^mt-related classification and prognostic signature could assist in determining the prognosis and personalized therapy of HCC patients from the perspectives of predictive, preventative and personalized medicine.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 5-6","pages":"768 - 784"},"PeriodicalIF":6.1,"publicationDate":"2024-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140139852","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 self-amplifying loop of TP53INP1 and P53 drives oxidative stress-induced apoptosis of bone marrow mesenchymal stem cells","authors":"Fanchao Li,&nbsp;Fei Zhang,&nbsp;Tao Wang,&nbsp;Zhihong Xie,&nbsp;Hong Luo,&nbsp;Wentao Dong,&nbsp;Jian Zhang,&nbsp;Chao Ren,&nbsp;Wuxun Peng","doi":"10.1007/s10495-023-01934-1","DOIUrl":"10.1007/s10495-023-01934-1","url":null,"abstract":"<div><p>Bone marrow mesenchymal stem cell (BMSC) transplantation is a promising regenerative therapy; however, the survival rate of BMSCs after transplantation is low. Oxidative stress is one of the main reasons for the high apoptosis rate of BMSCs after transplantation, so there is an urgent need to explore the mechanism of oxidative stress-induced apoptosis of BMSCs. Our previous transcriptome sequencing results suggested that the expression of P53-induced nuclear protein 1 (TP53INP1) and the tumor suppressor P53 (P53) was significantly upregulated during the process of oxidative stress-induced apoptosis of BMSCs. The present study further revealed the role and mechanism of TP53INP1 and P53 in oxidative stress-induced apoptosis in BMSCs. Overexpression of TP53INP1 induced apoptosis of BMSCs, knockdown of TP53INP1 alleviated oxidative stress apoptosis of BMSCs. Under oxidative stress conditions, P53 is regulated by TP53INP1, while P53 can positively regulate the expression of TP53INP1, so the two form a positive feedback loop. To clarify the mechanism of feedback loop formation. We found that TP53INP1 inhibited the ubiquitination and degradation of P53 by increasing the phosphorylation level of P53, leading to the accumulation of P53 protein. P53 can act on the promoter of the <i>TP53INP1</i> gene and increase the expression of <i>TP53INP1</i> through transcriptional activation. This is the first report on a positive feedback loop formed by TP53INP1 and P53 under oxidative stress. The present study clarified the formation mechanism of the positive feedback loop. The TP53INP1–P53 positive feedback loop may serve as a potential target for inhibiting oxidative stress-induced apoptosis in BMSCs.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 5-6","pages":"882 - 897"},"PeriodicalIF":6.1,"publicationDate":"2024-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11055765/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140139853","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":"FAM83B regulates mitochondrial metabolism and anti-apoptotic activity in pulmonary adenocarcinoma","authors":"Jiajia Wang,&nbsp;Panpan Li,&nbsp;Limin Sun,&nbsp;Jing Zhang,&nbsp;Ke Yue,&nbsp;Yan Wang,&nbsp;Xiaojuan Wu","doi":"10.1007/s10495-024-01944-7","DOIUrl":"10.1007/s10495-024-01944-7","url":null,"abstract":"","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 5-6","pages":"743 - 756"},"PeriodicalIF":6.1,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140118557","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":"Loss of AR-regulated AFF3 contributes to prostate cancer progression and reduces ferroptosis sensitivity by downregulating ACSL4 based on single-cell sequencing analysis","authors":"Aoyu Fan,&nbsp;Yunpeng Li,&nbsp;Yunyan Zhang,&nbsp;Wei Meng,&nbsp;Wei Pan,&nbsp;Meixi Chen,&nbsp;Zhongliang Ma,&nbsp;Wei Chen","doi":"10.1007/s10495-024-01941-w","DOIUrl":"10.1007/s10495-024-01941-w","url":null,"abstract":"<div><p>Prostate cancer (PCa) is one of the most common cancers affecting the health of men worldwide. Castration-resistant prostate cancer (CRPC), the advanced and refractory phase of prostate cancer, has multiple mechanisms of resistance to androgen deprivation therapy (ADT) such as AR mutations, aberrant androgen synthase, and abnormal expression of AR-related genes. Based on the research of the AR pathway, new drugs for the treatment of CRPC have been developed in clinical practice, such as Abiraterone and enzalutamide. However, many areas in this pathway are still worth exploring. In this study, single-cell sequencing analysis was utilized to scrutinize significant genes in the androgen receptor (AR) pathway related to CRPC. Our analysis of single-cell sequencing combined with bulk-cell sequencing revealed a substantial downregulation of AR-regulated AFF3 in CRPC. Overexpression of AFF3 restricted the proliferation and migration of prostate cancer cells whilst also increasing their sensitivity towards enzalutamide, while knockdown of AFF3 had the opposite effect. To elucidate the mechanism of tumor inhibition by AFF3, we applied GSVA and GSEA to investigate the metabolic pathways related to AFF3 and revealed that AFF3 had an impact on fatty acids metabolism and ferroptosis through the regulation of ACSL4 protein expression. Based on correlation analysis and flow cytometry, we can speculate that AFF3 can impact the sensitivity of the CRPC cell lines to the ferroptosis inducer (RSL3) by regulating ACSL4. Therefore, our findings may provide new insights into the mechanisms of drug resistance in CRPC, and AFF3 may serve as a novel prognostic biomarker in prostate cancer.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 9-10","pages":"1679 - 1695"},"PeriodicalIF":6.1,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140118558","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":"Analysis and experimental validation of necroptosis-related molecular classification, immune signature and feature genes in Alzheimer’s disease","authors":"Piaopiao Lian,&nbsp;Xing Cai,&nbsp;Xiaoman Yang,&nbsp;Zhuoran Ma,&nbsp;Cailin Wang,&nbsp;Ke Liu,&nbsp;Yi Wu,&nbsp;Xuebing Cao,&nbsp;Yan Xu","doi":"10.1007/s10495-024-01943-8","DOIUrl":"10.1007/s10495-024-01943-8","url":null,"abstract":"<div><p>Necroptosis, a programmed cell death pathway, has been demonstrated to be activated in Alzheimer’s disease (AD). However, the precise role of necroptosis and its correlation with immune cell infiltration in AD remains unclear. In this study, we conducted non-negative matrix factorization clustering analysis to identify three subtypes of AD based on necroptosis-relevant genes. Notably, these subtypes exhibited varying necroptosis scores, clinical characteristics and immune infiltration signatures. Cluster B, characterized by high necroptosis scores, showed higher immune cell infiltration and was associated with a more severe pathology, potentially representing a high-risk subgroup. To identify potential biomarkers for AD within cluster B, we employed two machine learning algorithms: the least absolute shrinkage and selection operator regression and Random Forest. Subsequently, we identified eight feature genes (CARTPT, KLHL35, NRN1, NT5DC3, PCYOX1L, RHOQ, SLC6A12, and SLC38A2) that were utilized to develop a diagnosis model with remarkable predictive capacity for AD. Moreover, we conducted validation using bulk RNA-seq, single-nucleus RNA-seq, and in vivo experiments to confirm the expression of these feature genes. In summary, our study identified a novel necroptosis-related subtype of AD and eight diagnostic biomarkers, explored the roles of necroptosis in AD progression and shed new light for the clinical diagnosis and treatment of this disease.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 5-6","pages":"726 - 742"},"PeriodicalIF":6.1,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11055779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140118616","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":"Circ_0098823 binding with IGF2BP3 regulates DNM1L stability to promote metastasis of hepatocellular carcinoma via mitochondrial fission","authors":"Jiuliang Yan,&nbsp;Xiaofeng Wang,&nbsp;Zongyu Fan,&nbsp;Yiqing Xu,&nbsp;Yingzi Zhang,&nbsp;Yi Liu,&nbsp;Lei Guo,&nbsp;Dongli Liu","doi":"10.1007/s10495-023-01903-8","DOIUrl":"10.1007/s10495-023-01903-8","url":null,"abstract":"<div><p>Hepatocellular carcinoma (HCC) is highly metastatic and invasive. CircRNA participates in gene regulation of multiple tumor metastases, but little is known whether it is a bystander or an actual player in HCC metastasis. We aim to explore the molecular mechanisms of novel circRNAs in HCC metastasis. RT-qPCR was used to detect the expression of 13 circRNAs derived by the ERBB3 gene. The function of circ_0098823 and DNM1L in HCC cells were estimated by CCK-8, transwell assays, flow cytometry, electron microscope, and in vivo experiments. RNA binding protein of circ_0098823 was confirmed by RNA pull-down, mass spectrometry, and RNA immunoprecipitation. The expression of DNM1L after IGF2BP3 knockdown was detected by RT-qPCR and western blot. Circ_0098823 was significantly up-regulated both in HCC tissues and HGF induced cell lines. Circ_0098823 overexpression significantly enhanced proliferation, migration, and invasion but decreased apoptosis of HCC cells, particularly promoted mitochondrial fission. Compared with the control group, the tumors in the circ_0098823 knockdown mice were significantly smaller and lighter. Circ_0098823 silencing suppressed DNM1L expression, a key molecule for fission, which enhanced proliferation, migration and invasion, and inhibited apoptosis of HCC cell. IGF2BP3 was a binding protein of circ_0098823. The expression and mRNA stability of DNM1L were down-regulated by IGF2BP3 knockdown. IGF2BP3 knockdown significantly alleviated the excessive migration, invasion and apoptosis of HCC cells caused by circ_0098823 overexpression. This study uncovered a novel circ_0098823 with tumor-promoting effect, and the mechanism by which circ_0098823 participates in HCC progression through IGF2BP3-guided DNM1L. Our study broadens molecular understanding of HCC progression.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 5-6","pages":"709 - 725"},"PeriodicalIF":6.1,"publicationDate":"2024-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140064691","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":"Apoptosis and pyroptosis in the nasal mucosa of Syrian hamster during SARS-CoV-2 infection and reinfection","authors":"Heng Li,&nbsp;Xin Zhao,&nbsp;Xinglong Zhang,&nbsp;Huiwen Zheng,&nbsp;Yibin Wang,&nbsp;Jinghan Hou,&nbsp;Jing Li,&nbsp;Yurong Zhao,&nbsp;Shasha Peng,&nbsp;Yingyan Li,&nbsp;Xin Zhang,&nbsp;Yifan Zhang,&nbsp;Jinling Yang,&nbsp;Zihan Zhang,&nbsp;Haijing Shi,&nbsp;Longding Liu","doi":"10.1007/s10495-024-01940-x","DOIUrl":"10.1007/s10495-024-01940-x","url":null,"abstract":"<div><p>In SARS-CoV-2 infection, it has been observed that viral replication lasts longer in the nasal mucosa than in the lungs, despite the presence of a high viral load at both sites. In hamsters, we found that the nasal mucosa exhibited a mild inflammatory response and minimal pathological injuries, whereas the lungs displayed a significant inflammatory response and severe injuries. The underlying cellular events may be induced by viral infection in three types of cell death: apoptosis, pyroptosis, and necroptosis. Our findings indicate that apoptosis was consistently activated during infection in the nasal mucosa, and the levels of apoptosis were consistent with the viral load. On the other hand, pyroptosis and a few instances of necroptosis were observed only on 7 dpi in the nasal mucosa. In the lungs, however, both pyroptosis and apoptosis were prominently activated on 3 dpi, with lower levels of apoptosis compared to the nasal mucosa. Interestingly, in reinfection, obvious viral load and apoptosis in the nasal mucosa were detected on 3 dpi, while no other forms of cell death were detected. We noted that the inflammatory reactions and pathological injuries in the nasal mucosa were milder, indicating that apoptosis may play a role in promoting lower inflammatory reactions and milder pathological injuries and contribute to the generation of long-term viral replication in the nasal mucosa. Our study provides valuable insights into the differences in cellular mechanisms during SARS-CoV-2 infection and highlights the potential significance of apoptosis regulation in the respiratory mucosa for controlling viral replication.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 7-8","pages":"1246 - 1259"},"PeriodicalIF":6.1,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139982210","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":"Retraction Note: Mahanine synergistically enhances cytotoxicity of 5-fluorouracil through ROS-mediated activation of PTEN and p53/p73 in colon carcinoma","authors":"Ranjita Das,&nbsp;Kaushik Bhattacharya,&nbsp;Sayantani Sarkar,&nbsp;Suman Kumar Samanta,&nbsp;Bikas C. Pal,&nbsp;Chitra Mandal","doi":"10.1007/s10495-024-01951-8","DOIUrl":"10.1007/s10495-024-01951-8","url":null,"abstract":"","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 5-6","pages":"569 - 569"},"PeriodicalIF":6.1,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139982211","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}