The Experts below are selected from a list of 574059 Experts worldwide ranked by ideXlab platform
Guido Kroemer - One of the best experts on this subject based on the ideXlab platform.
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The molecular machinery of regulated Cell Death
Cell Research, 2019Co-Authors: Daolin Tang, Tom Vanden Berghe, Peter Vandenabeele, Rui Kang, Guido KroemerAbstract:Cells may die from accidental Cell Death (ACD) or regulated Cell Death (RCD). ACD is a biologically uncontrolled process, whereas RCD involves tightly structured signaling cascades and molecularly defined effector mechanisms. A growing number of novel non-apoptotic forms of RCD have been identified and are increasingly being implicated in various human pathologies. Here, we critically review the current state of the art regarding non-apoptotic types of RCD, including necroptosis, pyroptosis, ferroptosis, entotic Cell Death, netotic Cell Death, parthanatos, lysosome-dependent Cell Death, autophagy-dependent Cell Death, alkaliptosis and oxeiptosis. The in-depth comprehension of each of these lethal subroutines and their interCellular consequences may uncover novel therapeutic targets for the avoidance of pathogenic Cell loss.
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immunogenic and tolerogenic Cell Death
Nature Reviews Immunology, 2009Co-Authors: Douglas R Green, Guido Kroemer, Thomas A Ferguson, Laurence ZitvogelAbstract:The immune system is routinely exposed to dead Cells during normal Cell turnover, injury and infection. Mechanisms must exist to discriminate between different forms of Cell Death in order to correctly eliminate pathogens and promote healing while avoiding responses to self, which can result in autoimmunity. However, an effective response against host tissue is also often needed to eliminate tumors following treatment with chemotherapeutic agents that trigger tumor Cell Death. Consequently, a central problem in immunology is to understand how the immune system determines whether Cell Death is immunogenic, tolerogenic or 'silent'.
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autophagic Cell Death the story of a misnomer
Nature Reviews Molecular Cell Biology, 2008Co-Authors: Guido Kroemer, Beth LevineAbstract:Dying Cells often display a large-scale accumulation of autophagosomes and hence adopt a morphology called autophagic Cell Death. In many cases, it is agreed that this autophagic Cell Death is Cell Death with autophagy rather than Cell Death by autophagy. Here, we evaluate the accumulating body of literature that argues that Cell Death occurs by autophagy. We also list the caveats that must be considered when deciding whether or not autophagy is an important effector mechanism of Cell Death.
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mitochondrial membrane permeabilization in Cell Death
Physical Review, 2007Co-Authors: Guido Kroemer, Lorenzo Galluzzi, Catherine BrennerAbstract:Irrespective of the morphological features of end-stage Cell Death (that may be apoptotic, necrotic, autophagic, or mitotic), mitochondrial membrane permeabilization (MMP) is frequently the decisive event that delimits the frontier between survival and Death. Thus mitochondrial membranes constitute the battleground on which opposing signals combat to seal the Cell's fate. Local players that determine the propensity to MMP include the pro- and antiapoptotic members of the Bcl-2 family, proteins from the mitochondrialpermeability transition pore complex, as well as a plethora of interacting partners including mitochondrial lipids. Intermediate metabolites, redox processes, sphingolipids, ion gradients, transcription factors, as well as kinases and phosphatases link lethal and vital signals emanating from distinct subCellular compartments to mitochondria. Thus mitochondria integrate a variety of proapoptotic signals. Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria. These catabolic enzymes as well as the cessation of the bioenergetic and redox functions of mitochondria finally lead to Cell Death, meaning that mitochondria coordinate the late stage of Cellular demise. Pathological Cell Death induced by ischemia/reperfusion, intoxication with xenobiotics, neurodegenerative diseases, or viral infection also relies on MMP as a critical event. The inhibition of MMP constitutes an important strategy for the pharmaceutical prevention of unwarranted Cell Death. Conversely, induction of MMP in tumor Cells constitutes the goal of anticancer chemotherapy.
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classification of Cell Death recommendations of the nomenclature committee on Cell Death
Cell Death & Differentiation, 2005Co-Authors: Guido Kroemer, Peter Vandenabeele, Wafik S Eldeiry, Pierre Golstein, Marcus E Peter, David L Vaux, Boris Zhivotovsky, Mikhail V Blagosklonny, Walter Malorni, Richard A KnightAbstract:Different types of Cell Death are often defined by morphological criteria, without a clear reference to precise biochemical mechanisms. The Nomenclature Committee on Cell Death (NCCD) proposes unified criteria for the definition of Cell Death and of its different morphologies, while formulating several caveats against the misuse of words and concepts that slow down progress in the area of Cell Death research. Authors, reviewers and editors of scientific periodicals are invited to abandon expressions like 'percentage apoptosis' and to replace them with more accurate descriptions of the biochemical and Cellular parameters that are actually measured. Moreover, at the present stage, it should be accepted that caspase-independent mechanisms can cooperate with (or substitute for) caspases in the execution of lethal signaling pathways and that 'autophagic Cell Death' is a type of Cell Death occurring together with (but not necessarily by) autophagic vacuolization. This study details the 2009 recommendations of the NCCD on the use of Cell Death-related terminology including 'entosis', 'mitotic catastrophe', 'necrosis', 'necroptosis' and 'pyroptosis'.
Seiji Kondo - One of the best experts on this subject based on the ideXlab platform.
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arsenic trioxide induces autophagic Cell Death in malignant glioma Cells by upregulation of mitochondrial Cell Death protein bnip3
Oncogene, 2005Co-Authors: Takao Kanzawa, Li Zhang, Lianchun Xiao, Isabelle M Germano, Yasuko Kondo, Seiji KondoAbstract:Arsenic trioxide induces autophagic Cell Death in malignant glioma Cells by upregulation of mitochondrial Cell Death protein BNIP3
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pivotal role of the Cell Death factor bnip3 in ceramide induced autophagic Cell Death in malignant glioma Cells
Cancer Research, 2004Co-Authors: Shigeru Daido, Takao Kanzawa, Yasuko Kondo, Akitsugu Yamamoto, Hayato Takeuchi, Seiji KondoAbstract:The sphingolipid ceramide has been recognized as an important second messenger implicated in regulating diverse signaling pathways especially for apoptosis. Very little is known, however, about the molecular mechanisms underlying nonapoptotic Cell Death induced by ceramide. In the present study, we first demonstrate that ceramide induces nonapoptotic Cell Death in malignant glioma Cells. The Cell Death was accompanied by several specific features characteristic of autophagy: presence of numerous autophagic vacuoles in the cytoplasm, development of the acidic vesicular organelles, autophagosome membrane association of microtubule-associated protein light chain 3 (LC3), and a marked increase in expression levels of two forms of LC3 protein (LC3-I and LC3-II). We additionally demonstrate that ceramide decreases mitochondrial membrane potential and activates the transcription of Death-inducing mitochondrial protein, BNIP3, resulting in increased expression levels of its mRNA and protein in malignant glioma Cells. Moreover, tumor Cells transfected with BNIP3 gene undergo autophagy in the absence of ceramide. These results suggest that ceramide induces autophagic Cell Death in malignant glioma Cells via activation of BNIP3. This study adds a new concept to characterize the pathways by which ceramide acts to induce nonapoptotic autophagic Cell Death in malignant gliomas.
John C Reed - One of the best experts on this subject based on the ideXlab platform.
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er stress induced Cell Death mechanisms
Biochimica et Biophysica Acta, 2013Co-Authors: Renata Sano, John C ReedAbstract:The endoplasmic-reticulum (ER) stress response constitutes a Cellular process that is triggered by a variety of conditions that disturb folding of proteins in the ER. Eukaryotic Cells have developed an evolutionarily conserved adaptive mechanism, the unfolded protein response (UPR), which aims to clear unfolded proteins and restore ER homeostasis. In cases where ER stress cannot be reversed, Cellular functions deteriorate, often leading to Cell Death. Accumulating evidence implicates ER stress-induced Cellular dysfunction and Cell Death as major contributors to many diseases, making modulators of ER stress pathways potentially attractive targets for therapeutics discovery. Here, we summarize recent advances in understanding the diversity of molecular mechanisms that govern ER stress signaling in health and disease. This article is part of a Special Section entitled: Cell Death Pathways.
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er stress induced Cell Death mechanisms
Biochimica et Biophysica Acta, 2013Co-Authors: Renata Sano, John C ReedAbstract:Abstract The endoplasmic-reticulum (ER) stress response constitutes a Cellular process that is triggered by a variety of conditions that disturb folding of proteins in the ER. Eukaryotic Cells have developed an evolutionarily conserved adaptive mechanism, the unfolded protein response (UPR), which aims to clear unfolded proteins and restore ER homeostasis. In cases where ER stress cannot be reversed, Cellular functions deteriorate, often leading to Cell Death. Accumulating evidence implicates ER stress-induced Cellular dysfunction and Cell Death as major contributors to many diseases, making modulators of ER stress pathways potentially attractive targets for therapeutics discovery. Here, we summarize recent advances in understanding the diversity of molecular mechanisms that govern ER stress signaling in health and disease. This article is part of a Special Section entitled: Cell Death Pathways. Guest Editors: Frank Madeo and Slaven Stekovic.
Junying Yuan - One of the best experts on this subject based on the ideXlab platform.
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systematic metrics depicting Cell Death kinetics
Chemistry & Biology, 2017Co-Authors: Junying YuanAbstract:In a recent issue of Cell Systems, Forcina et al. (2017) developed a scalable time-lapse analysis of Cell Death kinetics (STACK) method and combined it with a "lag exponential Death" model to quantitatively characterize the onset and rate of Cell Death. STACK provides a useful quantitative tool to determine how Cell Death kinetics may be modulated pharmacologically in Cell culture systems.
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expansion and evolution of Cell Death programmes
Nature Reviews Molecular Cell Biology, 2008Co-Authors: Alexei Degterev, Junying YuanAbstract:Cell Death has historically been divided into regulated (apoptotic) and unregulated (necrotic) mechanisms. Emerging evidence, however, suggests that these two categories do not adequately explain all Cell Death mechanisms. How and why might non-apoptotic, regulated Cell Death mechanisms have evolved?
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diversity in the mechanisms of neuronal Cell Death
Neuron, 2003Co-Authors: Junying Yuan, Marta M Lipinski, Alexei DegterevAbstract:Neurons may die as a normal physiological process during development or as a pathological process in diseases. The best-understood mechanism of neuronal Cell Death is apoptosis, which is regulated by an evolutionarily conserved Cellular pathway that consists of the caspase family, the Bcl-2 family, and the adaptor protein Apaf-1. Apoptosis, however, may not be the only Cellular mechanism that regulates neuronal Cell Death. Neuronal Cell Death may exhibit morphological features of autophagy or necrosis, which differ from that of the canonical apoptosis. This review evaluates the evidence supporting the existence of alternative mechanisms of neuronal Cell Death and proposes the possible existence of an evolutionarily conserved pathway of necrosis.
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mechanisms and functions of Cell Death
Annual Review of Cell Biology, 1991Co-Authors: R E Ellis, Junying Yuan, H R HorvitzAbstract:CONTENTS INTRODUCTION . . . . . . . . ... . . ... . . . . . . . . . . . . . . . ... . . . . . . . . . . . ...... . ... ... . . . . . . . . . . . . . . . ... ....... ... . . . . . . . . . . . ... . . ... . . . . . 664 Cell Death IN CAENORHABDITIS ELEGANS .... .. ..... . . . . 664 Programmed Cell Death . ... . . . . . . . . ... . . . . . ... . . . . . . . . . . . . . . . .. . . . . . . 665 Pathological Cell Deaths ....... . ........ ... . . . . . . . . . . . . . . .. . . . . . . . .. . . . . . . . . . . . . . . . . . . ........ 669 Summary . ... . . . . . . . . . .. .. '" . . .. . . . ... .... . . . . . .... . . ..... . . . ....... . . . . . . . . . . .. . . . . . . . . . . . . ...... 670 Cell Death IN OTHER ANIMALS .. . .. . . . . . . . . . . . . . . . . . . . . . . .. .. .. . ... . . . ... . . . ... . . ... . . . . . . . .. ... . . . . ... . . . ... ...... 670 Cell Death During the Metamorphosis of Moths. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . . . . . . . . . . . . . . . . 671 Deaths of Vertebrate Neurons Deprived of Growth Factors . . . ...... .... . . . . . ...... ... . 673 Cell Death ol'lhymocytes . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . . ... . . . . . . . . . . . . ..... . ... . . . . . . . . . . . . . . . . . . .. . ... . . . . . ... 675 Cell Death in the Regressing Rat Prostate ........ . 678 FUNCTIONS OF Cell Death 679 Cells That Appear to Have No Function .. ..... . . .... . . . . .... . ...... 680 Cells That Are Generated in Excess ......... ......... . . . . . . . . . . . 683 Cells That Develop Improperly . .. . . . .. . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . .. .. . . ....... ... .. . ... . . ...... 684 Cells That Have Completed Their Functions . . . . . . . . . .... . . ... . . . . . . . . . . . ... . . . . . . ... ... .. . . .. ... .. . . ... . 684 Cells That Are Harmful 685 MECHANISMS OF Cell Death 685 Cell Death Is an Active Process . . . .. . . ... . . . . . . . . ... . ...... . . .. 685 Control of the Cell Death Process ....... . 686 Mechanisms That Kill Cells . . . ... . . ... . ... . . . . . . . . . ... . . ... . ... . . . . . . .. . . . .. .. .... . . . . . . . .. 687 Engulfment of Dead Cells . . . ....... . . . . . . . 689 Degradation of Dead Cells. . . . . . . ... ... . . . . . . . .. . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . ... . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . 690 Future Prospects 690
Takao Kanzawa - One of the best experts on this subject based on the ideXlab platform.
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arsenic trioxide induces autophagic Cell Death in malignant glioma Cells by upregulation of mitochondrial Cell Death protein bnip3
Oncogene, 2005Co-Authors: Takao Kanzawa, Li Zhang, Lianchun Xiao, Isabelle M Germano, Yasuko Kondo, Seiji KondoAbstract:Arsenic trioxide induces autophagic Cell Death in malignant glioma Cells by upregulation of mitochondrial Cell Death protein BNIP3
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pivotal role of the Cell Death factor bnip3 in ceramide induced autophagic Cell Death in malignant glioma Cells
Cancer Research, 2004Co-Authors: Shigeru Daido, Takao Kanzawa, Yasuko Kondo, Akitsugu Yamamoto, Hayato Takeuchi, Seiji KondoAbstract:The sphingolipid ceramide has been recognized as an important second messenger implicated in regulating diverse signaling pathways especially for apoptosis. Very little is known, however, about the molecular mechanisms underlying nonapoptotic Cell Death induced by ceramide. In the present study, we first demonstrate that ceramide induces nonapoptotic Cell Death in malignant glioma Cells. The Cell Death was accompanied by several specific features characteristic of autophagy: presence of numerous autophagic vacuoles in the cytoplasm, development of the acidic vesicular organelles, autophagosome membrane association of microtubule-associated protein light chain 3 (LC3), and a marked increase in expression levels of two forms of LC3 protein (LC3-I and LC3-II). We additionally demonstrate that ceramide decreases mitochondrial membrane potential and activates the transcription of Death-inducing mitochondrial protein, BNIP3, resulting in increased expression levels of its mRNA and protein in malignant glioma Cells. Moreover, tumor Cells transfected with BNIP3 gene undergo autophagy in the absence of ceramide. These results suggest that ceramide induces autophagic Cell Death in malignant glioma Cells via activation of BNIP3. This study adds a new concept to characterize the pathways by which ceramide acts to induce nonapoptotic autophagic Cell Death in malignant gliomas.
