检索结果-南通市图书馆

A new cell death program regulated by toll-like receptor 9 through p38 mitogen-activated protein kinase signaling pathway in a neonatal rat model with sepsis associated encephalopathy

引用

Chinese Medical Journal 2022年第12期135卷 1474-1485页

作者： Ruixi Zhou Junjie Ying Xia Qiu Luting Yu Yan Yue Qian Liu Jing Shi Xihong Li Yi Qu Dezhi Mu Department of Pediatrics West China Second University HospitalSichuan UniversityChengduSichuan 610041China Key Laboratory of Birth Defects and Related Diseases of Women and Children Sichuan UniversityMinistry of EducationChengduSichuan 610041China

Background:Sepsis,a serious condition with high mortality,usually causes sepsis associated encephalopathy(SAE)that involves neuronal cell death.However,the cell death programs involved and their underlying mechanisms are not clear.This study aimed to explore the regulatory mechanisms of different cell death programs in SAE.Methods:A neonatal rat model of SAE was established by cecal ligation and perforation.Survival rate and vital signs(mean arterial pressure and heart rate)were monitored,nerve reflexes were evaluated,and cortical pathological changes were observed by hematoxylin and eosin staining.The expression of pyroptosis,apoptosis,and necroptosis(PANoptosis)-related proteins,mitogen-activated protein kinase(MAPK),and its upstream regulator toll-like receptor 9(TLR9)were detected.The expression of TLR9 in neurons was observed by immunofluorescence staining.The ultrastructure of neurons was observed by transmission electron microscope.Results:First,PANoptosis was found in cortical nerve cells of the SAE rats.Meanwhile,the subunits of MAPKs,p38 MAPK,Jun N-terminal kinase,and extracellular signal-regulated kinase(ERK)were activated.After pharmacologically inhibiting each of the subunits,only p38 MAPK was found to be associated with PANoptosis.Furthermore,blocking the p38 MAPK signaling pathway activated necroptosis but inhibited apoptosis and pyroptosis.When necroptosis was pharmacologically inhibited,apoptosis and pyroptosis were reactivated.Finally,we found that the expression of TLR9,a regulator of MAPKs,was significantly increased in this model.After down-regulation of TLR9,p38 MAPK,and ERK signaling pathways were inhibited,which led to the inhibition of PANoptosis.Further analysis found that down-regulation of TLR9 improved the survival rate and reduced the pathological changes in SAE rats.Conclusions:Our study showed that the programs comprising PANoptosis are activated simultaneously in SAE rats.TLR9 activated PANoptosis through the p38 MAPK signaling pathway.TLR9 may work as a potential target for SAE t

关键词： Sepsis associated encephalopathy TLR9 Apoptosis Pyroptosis necroptosis p38 mitogen-activated protein kinase

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Regulated cell death in cancer:from pathogenesis to treatment

引用

Chinese Medical Journal 2023年第6期136卷 653-665页

作者： Linjing Gong Dong Huang Yujun Shi Zong’an Liang Hong Bu Department of Respiratory and Critical Care Medicine West China HospitalSichuan UniversityChengduSichuan 610041China Institute of Clinical Pathology Key Laboratory of Transplant Engineering and ImmunologyNHCWest China HospitalSichuan UniversityChengduSichuan 610041China Department of Pathology West China HospitalSichuan UniversityChengduSichuan 610041China

Regulated cell death(RCD),including apoptosis,pyroptosis,necroptosis,and ferroptosis,is regulated by a series of evolutionarily conserved pathways,and is required for development and tissue homeostasis.Based on previous genetic and biochemical explorations of cell death subroutines,the characteristics of each are generally considered distinctive.However,recent in-depth studies noted the presence of crosstalk between the different forms of RCD;hence,the concept of PANoptosis appeared.Cancer,a complex genetic disease,is characterized by stepwise deregulation of cell apoptosis and proliferation,with significant morbidity and mortality globally.At present,studies on the different RCD pathways,as well as the intricate relationships between different cell death subroutines,mainly focus on infectious diseases,and their roles in cancer remain unclear.As cancers are characterized by dysregulated cell death and inflammatory responses,most current treatment strategies aim to selectively induce cell death via different RCD pathways in cancer cells.In this review,we describe five types of RCD pathways in detail with respect to tumorigenesis and cancer progression.The potential value of some of these key effector molecules in tumor diagnosis and therapeutic response has also been raised.We then review and highlight recent progress in cancer treatment based on PANoptosis and ferroptosis induced by small-molecule compounds,immune checkpoint inhibitors,and nanoparticles.Together,these findings may provide meaningful evidence to fill in the gaps between cancer pathogenesis and RCD pathways to develop better cancer therapeutic strategies.

关键词： Anti-cancer therapy Apoptosis Cancer Programmed cell death Pyroptosis PANoptosis necroptosis Ferroptosis Diagnosis death Pyroptosis PANoptosis necroptosis Ferroptosis Diagnosis

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Preliminary evidence for the presence of multiple forms of cell death in diabetes cardiomyopathy

引用

Acta Pharmaceutica Sinica B 2022年第1期12卷 1-17页

作者： Jinjing Wei Yongting Zhao Haihai Liang Weijie Du Lihong Wang Department of Endocrinology the First Affiliated Hospital of Jinan UniversityGuangzhou 510630China Department of Endocrinology the Second Affiliated Hospital of Harbin Medical UniversityHarbin 150081China Department of Pharmacology(State-Province Key Laboratories of Biomedicine-Pharmaceutics of China Key Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin 150081China

Diabetic mellitus(DM) is a common degenerative chronic metabolic disease often accompanied by severe cardiovascular complications(DCCs) as major causes of death in diabetic patients with diabetic cardiomyopathy(DCM) as the most common DCC. The metabolic disturbance in DCM generates the conditions/substrates and inducers/triggers and activates the signaling molecules and death executioners leading to cardiomyocyte death which accelerates the development of DCM and the degeneration of DCM to heart failure.Various forms of programmed active cell death including apoptosis, pyroptosis, autophagic cell death, autosis,necroptosis, ferroptosis and entosis have been identified and characterized in many types of cardiac disease.Evidence has also been obtained for the presence of multiple forms of cell death in DCM. Most importantly,published animal experiments have demonstrated that suppression of cardiomyocyte death of any forms yields tremendous protective effects on DCM. Herein, we provide the most updated data on the subject of cell death in DCM, critical analysis of published results focusing on the pathophysiological roles of cell death, and pertinent perspectives of future studies.

关键词： Diabetes mellitus Diabetic cardiomyopathy Cell death Apoptosis Autophagic cell death Aautosis Pyroptosis necroptosis Ferroptosis

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Aging-elevated inflammation promotes DNMT3A R878H-driven clonal hematopoiesis

引用

Acta Pharmaceutica Sinica B 2022年第2期12卷 678-691页

作者： Min Liao Ruiqing Chen Yang Yang Hanqing He Liqian Xu Yuxuan Jiang Zhenxing Guo Wei He Hong Jiang Jianwei Wang School of Pharmaceutical Sciences Tsinghua UniversityBeijing 100084China Kidney Disease Center the First Affiliated HospitalCollege of MedicineZhejiang UniversityHangzhou 310003China Department of Hematology/Oncology First Hospital of Tsinghua UniversityBeijing 100016China

Aging-elevated DNMT3A R882H-driven clonal hematopoiesis(CH)is a risk factor for myeloid malignancies remission and overall survival.Although some studies were conducted to investigate this phenomenon,the exact mechanism is still under debate.In this study,we observed that DNMT3 A R878 H bone marrow cells(human allele:DNMT3 A R882 H)displayed enhanced reconstitution capacity in aged bone marrow milieu and upon inflammatory insult.DNMT3 A R878 H protects hematopoietic stem and progenitor cells from the damage induced by chronic inflammation,especially TNFa insults.Mechanistically,we identified that RIPK1-RIPK3-MLKL-mediated necroptosis signaling was compromised in R878 H cells in response to proliferation stress and TNFa insults.Briefly,we elucidated the molecular mechanism driving DNMT3 A R878 H-based clonal hematopoiesis,which raises clinical value for treating DNMT3 A R882 H-driven clonal hematopoiesis and myeloid malignancies with aging.

关键词： Aging Inflammation DNMT3A R882H Clonal hematopoiesis Hematopoietic stem cells necroptosis TNFα

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

The regulatory role of Pin1 in neuronal death

引用

Neural Regeneration Research 2023年第1期18卷 74-80页

作者： Shu-Chao Wang Xi-Min Hu Kun Xiong Center for Medical Research The Second Xiangya Hospital of Central South UniversityChangshaHunan ProvinceChina Department of Anatomy and Neurobiology School of Basic Medical SciencesCentral South UniversityChangshaHunan ProvinceChina Hunan Key Laboratory of Ophthalmology ChangshaHunan ProvinceChina

Regulated cell death predominantly involves apoptosis,autophagy,and regulated necrosis.It is vital that we understand how key regulatory signals can control the process of cell death.Pin1 is a cis-trans isomerase that catalyzes the isomerization of phosphorylated serine or threonine-proline motifs of a protein,thereby acting as a crucial molecular switch and regulating the protein functionality and the signaling pathways involved.However,we know very little about how Pin1-associated pathways might play a role in regulated cell death.In this paper,we review the role of Pin1 in regulated cell death and related research progress and summarize Pin1-related pathways in regulated cell death.Aside from the involvement of Pin1 in the apoptosis that accompanies neurodegenerative diseases,accumulating evidence suggests that Pin1 also plays a role in regulated necrosis and autophagy,thereby exhibiting distinct effects,including both neurotoxic and neuroprotective effects.Gaining an enhanced understanding of Pin1 in neuronal death may provide us with new options for the development of therapeutic target for neurodegenerative disorders.

关键词： apoptosis autophagy calpain central nervous system necroptosis necrosis neurodegenerative diseases neuron Pin1 regulated neuronal death

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

PANoptosis-like cell death in ischemia/reperfusion injury of retinal neurons

引用

Neural Regeneration Research 2023年第2期18卷 357-363页

作者： Wei-Tao Yan Wen-Juan Zhao Xi-Min Hu Xiao-Xia Ban Wen-Ya Ning Hao Wan Qi Zhang Kun Xiong Department of Human Anatomy and Neurobiology School of Basic Medical ScienceCentral South UniversityChangshaHunan ProvinceChina Department of Dermatology Xiangya HospitalCentral South UniversityChangshaHunan ProvinceChina Department of Human Resources Third Xiangya Hospital of Central South UniversityChangshaHunan ProvinceChina Hunan Key Laboratory of Ophthalmology ChangshaHunan ProvinceChina Key Laboratory of Emergency and Trauma Ministry of EducationCollege of Emergency and TraumaHainan Medical UniversityHaikouHainan ProvinceChina

PANoptosis is a newly identified type of regulated cell death that consists of pyroptosis,apoptosis,and nec roptosis,which simultaneously occur during the pathophysiological process of infectious and inflammatory diseases.Although our previous lite rature mining study suggested that PANoptosis might occur in neuronal ischemia/repe rfusion injury,little experimental research has been reported on the existence of PANoptosis.In this study,we used in vivo and in vitro retinal neuronal models of ischemia/repe rfusion injury to investigate whether PAN optosis-like cell death(simultaneous occurrence of pyroptosis,apo ptosis,and necroptosis)exists in retinal neuronal ischemia/repe rfusion injury.Our results showed that ischemia/repe rfusion injury induced changes in morphological features and protein levels that indicate PANoptosis-like cell death in retinal neurons both in vitro and in vivo.Ischemia/repe rfusion inju ry also significantly upregulated caspase-1,caspase-8,and NLRP3 expression,which are important components of the PANoptosome.These results indicate the existence of PANoptosis-like cell death in ischemia/reperfusion injury of retinal neurons and provide preliminary experimental evidence for future study of this new type of regulated cell death.

关键词： apoptosis gasdermin-D(GSDMD) ischemia/reperfusion mixed lineage kinase domain-like protein(MLKL) necroptosis NOD-like receptor protein 3(NLRP3) PANoptosis pyroptosis receptor-interacting protein kinase 3(RIPK3) retinal neuron

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Non-apoptotic cell death-based cancer therapy:Molecular mechanism,pharmacological modulators,and nanomedicine

引用

Acta Pharmaceutica Sinica B 2022年第9期12卷 3567-3593页

作者： Xuan Wang Peng Hua Chengwei He Meiwan Chen State Key Laboratory of Quality Research in Chinese Medicine Institute of Chinese Medical SciencesUniversity of MacaoMacaoSAR 999078China

As an emerging cancer therapeutic target,non-apoptotic cell death such as ferroptosis,necroptosis and pyroptosis,etc.,has revealed significant potential in cancer treatment for bypassing apoptosis to enhance the undermined therapeutic efficacy triggered by apoptosis resistance.A variety of anticancer drugs,synthesized compounds and natural products have been proven recently to induce non-apoptotic cell death and exhibit excellent anti-tumor effects.Moreover,the convergence of nanotechnology with functional materials and biomedicine science has provided tremendous opportunities to construct non-apoptotic cell death-based nanomedicine for innovative cancer therapy.Nanocarriers are not only employed in targeted delivery of non-apoptotic inducers,but also used as therapeutic components to induce non-apoptotic cell death to achieve efficient tumor treatment.This review first introduces the main characteristics,the mechanism and various pharmacological modulators of different non-apoptotic cell death forms,including ferroptosis,necroptosis,pyroptosis,autophagy,paraptosis,lysosomal-dependent cell death,and oncosis.Second,we comprehensively review the latest progresses of nanomedicine that induces various forms of non-apoptotic cell death and focus on the nanomedicine targeting different pathways and components.Furthermore,the combination therapies of non-apoptotic cell death with photothermal therapy,photodynamic therapy,immunotherapy and other modalities are summarized.Finally,the challenges and future perspectives in this regard are also discussed.

关键词： Non-apoptotic cell death Ferroptosis necroptosis Pyroptosis Autophagy Nanomedicine Combination therapies Anticancer

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Role of Receptor Interacting Protein(RIP)kinases in cancer

引用

Genes & Diseases 2022年第6期9卷 1579-1593页

作者： Kaylee Ermine Jian Yu Lin Zhang Department of Pharmacology and Chemical Biology University of Pittsburgh School of MedicinePittsburghPA 15213USA UPMC Hillman Cancer Center PittsburghPA 15213USA Department of Pathology University of Pittsburgh School of MedicinePittsburghPA 15213USA

The Receptor Interacting Protein(RIP)kinase family consists of seven Serine/Threonine kinases,which plays a key signaling role in cell survival and cell death.Each RIP family member contains a conserved kinase domain and other domains that determine the specific kinase function through proteineprotein interactions.RIP1 and RIP3 are best known for their critical roles in necroptosis,programmed necrosis and a non-apoptotic inflammatory cell death process.Dysregulation of RIP kinases contributes to a variety of pathogenic conditions such as inflammatory diseases,neurological diseases,and cancer.In cancer cells,alterations of RIP kinases at genetic,epigenetic and expression levels are frequently found,and suggested to promote tumor progression and metastasis,escape of antitumor immune response,and therapeutic resistance.However,RIP kinases can be either pro-tumor or anti-tumor depending on specific tumor types and cellular contexts.Therapeutic agents for targeting RIP kinases have been tested in clinical trials mainly for inflammatory diseases.Deregulated expression of these kinases in different types of cancer suggests that they represent attractive therapeutic targets.The focus of this review is to outline the role of RIP kinases in cancer,highlighting potential opportunities to manipulate these proteins in cancer treatment.

关键词： Cancer Cell death Immune response necroptosis RIP kinases

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

necroptosis:An emerging type of cell death in liver diseases

引用

World Journal of Gastroenterology 2014年第35期20卷 12526-12532页

作者： Waqar Khalid Saeed Dae Won Jun Department of Gastroenterology Hanyang University School of Medicine

Cell death has been extensively evaluated for decades and it is well recognized that pharmacological interventions directed to inhibit cell death can prevent significant cell loss and can thus improve an organ’s physiological function.For long,only apoptosis was considered as a sole form of programmed cell death.Recently necroptosis,a RIP1/RIP3-dependent programmed cell death,has been identified as an apoptotic backup cell death mechanism with necrotic morphology.The evidences of necroptosis and protective effects achieved by blocking necroptosis have been extensively reported in recent past.However,only a few studies reported the evidence of necroptosis and protective effects achieved by inhibiting necroptosis in liver related disease conditions.Although the number of necroptosis initiators is increasing;however,interestingly,it is still unclear that what actually triggers necroptosis in different liver diseases or if there is always a different necroptosis initiator in each specific disease condition followed by specific downstream signaling molecules.Understanding the precise mechanism of necroptosis as well as counteracting other cell death pathways in liver diseases could provide a useful insight towards achieving extensive therapeutic significance.By targeting necroptosis and/or other parallel death pathways,a significant cell loss and thus a decrement in an organ’s physiological function can be prevented.

关键词： necroptosis Programmed necrosis Apopto-sis Cell de

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Polo-like kinase 1 suppresses lung adenocarcinoma immunity throughnecroptosis

引用

肿瘤学研究(英文) 2023年第6期31卷 937-953页

作者： PENGCHENG ZHANG XINGLONG ZHANG YONGFU ZHU YIYI CUI JING XU WEIPING ZHANG Department of Oncology The Third Affiliated Hospital of Zhejiang Chinese Medical UniversityHangzhouChina Department of Oncology Anhui Zhongke Gengjiu HospitalHefeiChina Department of Oncology The First Affiliated Hospital of Anhui University of Chinese MedicineHefeiChina Department of Biochemistry and Molecular Biology School of Integrated Chinese and Western MedicineAnhui University of Chinese MedicineHefeiChina

Polo-like kinase 1(PLK1)plays a crucial role in cell mitosis and has been associated with necroptosis.However,the role of PLK1 and necroptosis in lung adenocarcinoma(LA)remains unclear.In this study,we analyzed The Cancer Genome Atlas(TCGA)and Genotype-Tissue Expression databases to evaluate the prognostic value and mechanistic role of PLK1 in LA.PLK1 was found to be highly expressed in LA and was positively associated with advanced disease staging and poor survival outcomes.Functional enrichment analysis showed that PLK1 was involved in cell mitosis,neurotransmitter transmission,and drug metabolism.Further analysis using single-sample gene set enrichment analysis and ESTIMATE algorithm revealed a correlation between PLK1 expression and immune infiltration in LA.Silencing of PLK1 using miRNA transfection in LA cells reduced cell proliferation and increased apoptosis,as well as upregulating the expression of necroptosis-related proteins,such as RIPK1,RIPK3,and MLKL.Additionally,nude mouse transplantation tumor experiments demonstrated that silencing PLK1 reduced the growth capacity of LA cells.These findings suggest that PLK1 plays a critical role in LA progression by regulating necroptosis and immune infiltration,and may serve as a potential therapeutic target for immunotherapy.Furthermore,PLK1 expression can be used as a prognostic biomarker for LA patients.

关键词： PLK1 Lung adenocarcinoma Prognosis biomarker Immune infiltration necroptosis

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：