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7 results on '"Juin, Philippe P."'

1. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Author

Galluzzi L, Vitale I, Aaronson SA, Abrams JM, Adam D, Agostinis P, Alnemri ES, Altucci L, Amelio I, Andrews DW, Annicchiarico-Petruzzelli M, Antonov AV, Arama E, Baehrecke EH, Barlev NA, Bazan NG, Bernassola F, Bertrand MJM, Bianchi K, Blagosklonny MV, Blomgren K, Borner C, Boya P, Brenner C, Campanella M, Candi E, Carmona-Gutierrez D, Cecconi F, Chan FK, Chandel NS, Cheng EH, Chipuk JE, Cidlowski JA, Ciechanover A, Cohen GM, Conrad M, Cubillos-Ruiz JR, Czabotar PE, D'Angiolella V, Dawson TM, Dawson VL, De Laurenzi V, De Maria R, Debatin KM, DeBerardinis RJ, Deshmukh M, Di Daniele N, Di Virgilio F, Dixit VM, Dixon SJ, Duckett CS, Dynlacht BD, El-Deiry WS, Elrod JW, Fimia GM, Fulda S, García-Sáez AJ, Garg AD, Garrido C, Gavathiotis E, Golstein P, Gottlieb E, Green DR, Greene LA, Gronemeyer H, Gross A, Hajnoczky G, Hardwick JM, Harris IS, Hengartner MO, Hetz C, Ichijo H, Jäättelä M, Joseph B, Jost PJ, Juin PP, Kaiser WJ, Karin M, Kaufmann T, Kepp O, Kimchi A, Kitsis RN, Klionsky DJ, Knight RA, Kumar S, Lee SW, Lemasters JJ, Levine B, Linkermann A, Lipton SA, Lockshin RA, López-Otín C, Lowe SW, Luedde T, Lugli E, MacFarlane M, Madeo F, Malewicz M, Malorni W, Manic G, Marine JC, Martin SJ, Martinou JC, Medema JP, Mehlen P, Meier P, Melino S, Miao EA, Molkentin JD, Moll UM, Muñoz-Pinedo C, Nagata S, Nuñez G, Oberst A, Oren M, Overholtzer M, Pagano M, Panaretakis T, Pasparakis M, Penninger JM, Pereira DM, Pervaiz S, Peter ME, Piacentini M, Pinton P, Prehn JHM, Puthalakath H, Rabinovich GA, Rehm M, Rizzuto R, Rodrigues CMP, Rubinsztein DC, Rudel T, Ryan KM, Sayan E, Scorrano L, Shao F, Shi Y, Silke J, Simon HU, Sistigu A, Stockwell BR, Strasser A, Szabadkai G, Tait SWG, Tang D, Tavernarakis N, Thorburn A, Tsujimoto Y, Turk B, Vanden Berghe T, Vandenabeele P, Vander Heiden MG, Villunger A, Virgin HW, Vousden KH, Vucic D, Wagner EF, Walczak H, Wallach D, Wang Y, Wells JA, Wood W, Yuan J, Zakeri Z, Zhivotovsky B, Zitvogel L, Melino G, and Kroemer G

Subjects
Animals, Humans, Lysosomes metabolism, Lysosomes pathology, Mitochondrial Membrane Transport Proteins metabolism, Mitochondrial Permeability Transition Pore, Necrosis metabolism, Necrosis pathology, Cell Death
Abstract

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

Published
2018
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2. E2F1 interacts with BCL-xL and regulates its subcellular localization dynamics to trigger cell death.

Author

Vuillier C, Lohard S, Fétiveau A, Allègre J, Kayaci C, King LE, Braun F, Barillé-Nion S, Gautier F, Dubrez L, Gilmore AP, Juin PP, and Maillet L

Subjects
Apoptosis, Cell Line, Tumor, E2F1 Transcription Factor chemistry, Extracellular Space metabolism, Gene Expression Regulation drug effects, Humans, Mitochondria metabolism, Protein Binding, Protein Transport, Proto-Oncogene Proteins c-bcl-2 genetics, Proto-Oncogene Proteins c-bcl-2 metabolism, Transcription, Genetic, bcl-2 Homologous Antagonist-Killer Protein metabolism, bcl-X Protein chemistry, Cell Death, E2F1 Transcription Factor metabolism, bcl-X Protein metabolism
Abstract

E2F1 is the main pro-apoptotic effector of the pRB-regulated tumor suppressor pathway by promoting the transcription of various pro-apoptotic proteins. We report here that E2F1 partly localizes to mitochondria, where it favors mitochondrial outer membrane permeabilization. E2F1 interacts with BCL-xL independently from its BH3 binding interface and induces a stabilization of BCL-xL at mitochondrial membranes. This prevents efficient control of BCL-xL over its binding partners, in particular over BAK resulting in the induction of cell death. We thus identify a new, non-BH3-binding regulator of BCL-xL localization dynamics that influences its anti-apoptotic activity., (© 2017 The Authors.)

Published
2018
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3. Keeping Cell Death Alive: An Introduction into the French Cell Death Research Network.

Author

Ichim, Gabriel, Gibert, Benjamin, Adriouch, Sahil, Brenner, Catherine, Davoust, Nathalie, Desagher, Solange, Devos, David, Dokudovskaya, Svetlana, Dubrez, Laurence, Estaquier, Jérôme, Gillet, Germain, Guénal, Isabelle, Juin, Philippe P., Kroemer, Guido, Legembre, Patrick, Levayer, Romain, Manon, Stéphen, Mehlen, Patrick, Meurette, Olivier, and Micheau, Olivier

Subjects
THANATOLOGY, CELL death, CANCER cells, CAENORHABDITIS elegans, NOBEL Prizes, APOPTOSIS
Abstract

Since the Nobel Prize award more than twenty years ago for discovering the core apoptotic pathway in C. elegans, apoptosis and various other forms of regulated cell death have been thoroughly characterized by researchers around the world. Although many aspects of regulated cell death still remain to be elucidated in specific cell subtypes and disease conditions, many predicted that research into cell death was inexorably reaching a plateau. However, this was not the case since the last decade saw a multitude of cell death modalities being described, while harnessing their therapeutic potential reached clinical use in certain cases. In line with keeping research into cell death alive, francophone researchers from several institutions in France and Belgium established the French Cell Death Research Network (FCDRN). The research conducted by FCDRN is at the leading edge of emerging topics such as non-apoptotic functions of apoptotic effectors, paracrine effects of cell death, novel canonical and non-canonical mechanisms to induce apoptosis in cell death-resistant cancer cells or regulated forms of necrosis and the associated immunogenic response. Collectively, these various lines of research all emerged from the study of apoptosis and in the next few years will increase the mechanistic knowledge into regulated cell death and how to harness it for therapy. [ABSTRACT FROM AUTHOR]

Published
2022
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4. STING-dependent paracriny shapes apoptotic priming of breast tumors in response to anti-mitotic treatment

Author

Lohard, Steven, Bourgeois, Nathalie, Maillet, Laurent, Gautier, Fabien, Fétiveau, Aurélie, Lasla, Hamza, Nguyen, Frédérique, Vuillier, Céline, Dumont, Alison, Moreau-Aubry, Agnès, Frapin, Morgane, David, Laurent, Loussouarn, Delphine, Kerdraon, Olivier, Campone, Mario, Jézéquel, Pascal, Juin, Philippe P., Barillé-Nion, Sophie, Stress Adaptation and Tumor Escape in Breast Cancer (CRCINA-ÉQUIPE 8), Centre de Recherche en Cancérologie et Immunologie Nantes-Angers (CRCINA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA), Site de Recherche Intégrée sur le Cancer - SIRIC « ILIAD » [Nantes] (INCA-DGOS-Inserm), Institut de Cancérologie de l'Ouest [Angers/Nantes] (UNICANCER/ICO), UNICANCER, Regulation of Bcl2 and p53 Networks in Multiple Myeloma and Mantle Cell Lymphoma (CRCINA-ÉQUIPE 10), Physiopathologie des Adaptations Nutritionnelles (PhAN), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Centre de Recherche en Transplantation et Immunologie (U1064 Inserm - CRTI), Université de Nantes (UN)-Université de Nantes (UN), Structure fédérative de recherche François Bonamy (SFR François Bonamy), Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche en Santé de l'Université de Nantes (IRS-UN), Service d'Anatomie Pathologique [CHU Nantes], Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre Hospitalier Universitaire G. R. Laennec (HGRL Saint-Herblain), This work was supported by the Ligue contre le Cancer (44, 22, 53, 56, and 85), the Canceropole Grand Ouest, the Region Pays de la Loire (MATURE project 2017–18) and the Agence Nationale de la Recherche (Grands defis societaux 2015–2020, Antinetrex project)., Stress Adaptation and Tumor Escape in breast cancer - SATE (CRCINA - Département ONCO - Equipe 8), Centre de recherche de Cancérologie et d'Immunologie / Nantes - Angers (CRCINA), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Institut de cancérologie de l'Ouest - Nantes (ICO Nantes), CRLCC Paul Papin-CRLCC René Gauducheau, Regulation of Bcl2 and p53 networks in Multiple Myeloma and Mantle Cell Lymphoma (CRCINA - Département NOHMAD - Equipe 10), Physiologie des Adaptations Nutritionnelles [UMR_A1280] (PhAN), Institut National de la Recherche Agronomique (INRA)-Université de Nantes (UN), Bernardo, Elizabeth, and Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)

Subjects
Cell death, Cell biology, Paclitaxel, Science, bcl-X Protein, Apoptosis, Breast Neoplasms, [SDV.CAN]Life Sciences [q-bio]/Cancer, Antimitotic Agents, Article, Cell Line, Gene Knockout Techniques, Mice, Breast cancer, [SDV.CAN] Life Sciences [q-bio]/Cancer, Paracrine Communication, Tumor Cells, Cultured, Animals, Humans, lcsh:Science, Cancer, Tumor Necrosis Factor-alpha, Membrane Proteins, Nucleotidyltransferases, Xenograft Model Antitumor Assays, Proto-Oncogene Proteins c-bcl-2, Interferon Type I, lcsh:Q, Female, Signal Transduction
Abstract

A fascinating but uncharacterized action of antimitotic chemotherapy is to collectively prime cancer cells to apoptotic mitochondrial outer membrane permeabilization (MOMP), while impacting only on cycling cell subsets. Here, we show that a proapoptotic secretory phenotype is induced by activation of cGAS/STING in cancer cells that are hit by antimitotic treatment, accumulate micronuclei and maintain mitochondrial integrity despite intrinsic apoptotic pressure. Organotypic cultures of primary human breast tumors and patient-derived xenografts sensitive to paclitaxel exhibit gene expression signatures typical of type I IFN and TNFα exposure. These cytokines induced by cGAS/STING activation trigger NOXA expression in neighboring cells and render them acutely sensitive to BCL-xL inhibition. cGAS/STING-dependent apoptotic effects are required for paclitaxel response in vivo, and they are amplified by sequential, but not synchronous, administration of BH3 mimetics. Thus anti-mitotic agents propagate apoptotic priming across heterogeneously sensitive cancer cells through cytosolic DNA sensing pathway-dependent extracellular signals, exploitable by delayed MOMP targeting., Antimitotic compounds, such as paclitaxel, induce cell death in cycling cancer cells only. Here, the authors show that paclitaxel-targeted breast cancer cells prime neighboring cells to apoptosis through a STING-mediated paracrine signaling pathway.

Published
2020
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5. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Author

Galluzzi, Lorenzo, Vitale, Ilio, Aaronson, Stuart A, Abrams, John M, Adam, Dieter, Agostinis, Patrizia, Alnemri, Emad S, Altucci, Lucia, Amelio, Ivano, Andrews, David W, Annicchiarico-Petruzzelli, Margherita, Antonov, Alexey V, Arama, Eli, Baehrecke, Eric H, Barlev, Nickolai A, Bazan, Nicolas G, Bernassola, Francesca, Bertrand, Mathieu JM, Bianchi, Katiuscia, Blagosklonny, Mikhail V, Blomgren, Klas, Borner, Christoph, Boya, Patricia, Brenner, Catherine, Campanella, Michelangelo, Candi, Eleonora, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K-M, Chandel, Navdeep S, Cheng, Emily H, Chipuk, Jerry E, Cidlowski, John A, Ciechanover, Aaron, Cohen, Gerald M, Conrad, Marcus, Cubillos-Ruiz, Juan R, Czabotar, Peter E, D'Angiolella, Vincenzo, Dawson, Ted M, Dawson, Valina L, De Laurenzi, Vincenzo, De Maria, Ruggero, Debatin, Klaus-Michael, DeBerardinis, Ralph J, Deshmukh, Mohanish, Di Daniele, Nicola, Di Virgilio, Francesco, Dixit, Vishva M, Dixon, Scott J, Duckett, Colin S, Dynlacht, Brian D, El-Deiry, Wafik S, Elrod, John W, Fimia, Gian Maria, Fulda, Simone, García-Sáez, Ana J, Garg, Abhishek D, Garrido, Carmen, Gavathiotis, Evripidis, Golstein, Pierre, Gottlieb, Eyal, Green, Douglas R, Greene, Lloyd A, Gronemeyer, Hinrich, Gross, Atan, Hajnoczky, Gyorgy, Hardwick, J Marie, Harris, Isaac S, Hengartner, Michael O, Hetz, Claudio, Ichijo, Hidenori, Jäättelä, Marja, Joseph, Bertrand, Jost, Philipp J, Juin, Philippe P, Kaiser, William J, Karin, Michael, Kaufmann, Thomas, Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N, Klionsky, Daniel J, Knight, Richard A, Kumar, Sharad, Lee, Sam W, Lemasters, John J, Levine, Beth, Linkermann, Andreas, Lipton, Stuart A, Lockshin, Richard A, López-Otín, Carlos, Lowe, Scott W, Luedde, Tom, Lugli, Enrico, MacFarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, and Manic, Gwenola

Subjects
Necrosis, Biochemistry & Molecular Biology, Cell Death, Mitochondrial Permeability Transition Pore, Animals, Humans, Biological Sciences, Lysosomes, Mitochondrial Membrane Transport Proteins, Medical and Health Sciences
Abstract

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

Published
2018

6. Targeting of BCL-2 Family Members during Anticancer Treatment: A Necessary Compromise between Individual Cell and Ecosystemic Responses?

Author

Barillé-Nion, Sophie, Lohard, Steven, and Juin, Philippe P.

Subjects
BCL-2 proteins, CELL death, CELL populations, CELL communication, CANCER cells
Abstract

The imbalance between BCL-2 homologues and pro-death counterparts frequently noted in cancer cells endows them with a cell autonomous survival advantage. To eradicate ectopic cells, inhibitors of these homologues (BH3 mimetics) were developed to trigger, during anticancer treatment, full activation of the canonical mitochondrial apoptotic pathway and related caspases. Despite efficiency in some clinical settings, these compounds do not completely fulfill their initial promise. We herein put forth that a growing body of evidence indicates that mitochondrial integrity, controlled by BCL-2 family proteins, and downstream caspases regulate other cell death modes and influence extracellular signaling by committed cells. Moreover, intercellular communications play a key role in spreading therapeutic response across cancer cell populations and in engaging an immune response. We thus advocate that BH3 mimetics administration would be more efficient in the long term if it did not induce apoptosis in all sensitive cells at the same time, but if it could instead allow (or trigger) death signal production by non-terminally committed dying cell populations. The development of such a trade-off strategy requires to unravel the effects of BH3 mimetics not only on each individual cancer cell but also on homotypic and heterotypic cell interactions in dynamic tumor ecosystems. [ABSTRACT FROM AUTHOR]

Published
2020
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7. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Author

Galluzzi, Lorenzo, Vitale, Ilio, Aaronson, Stuart A, Abrams, John M, Adam, Dieter, Agostinis, Patrizia, Alnemri, Emad S, Altucci, Lucia, Amelio, Ivano, Andrews, David W, Annicchiarico-Petruzzelli, Margherita, Antonov, Alexey V, Arama, Eli, Baehrecke, Eric H, Barlev, Nickolai A, Bazan, Nicolas G, Bernassola, Francesca, Bertrand, Mathieu JM, Bianchi, Katiuscia, Blagosklonny, Mikhail V, Blomgren, Klas, Borner, Christoph, Boya, Patricia, Brenner, Catherine, Campanella, Michelangelo, Candi, Eleonora, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K-M, Chandel, Navdeep S, Cheng, Emily H, Chipuk, Jerry E, Cidlowski, John A, Ciechanover, Aaron, Cohen, Gerald M, Conrad, Marcus, Cubillos-Ruiz, Juan R, Czabotar, Peter E, D'Angiolella, Vincenzo, Dawson, Ted M, Dawson, Valina L, De Laurenzi, Vincenzo, De Maria, Ruggero, Debatin, Klaus-Michael, DeBerardinis, Ralph J, Deshmukh, Mohanish, Di Daniele, Nicola, Di Virgilio, Francesco, Dixit, Vishva M, Dixon, Scott J, Duckett, Colin S, Dynlacht, Brian D, El-Deiry, Wafik S, Elrod, John W, Fimia, Gian Maria, Fulda, Simone, García-Sáez, Ana J, Garg, Abhishek D, Garrido, Carmen, Gavathiotis, Evripidis, Golstein, Pierre, Gottlieb, Eyal, Green, Douglas R, Greene, Lloyd A, Gronemeyer, Hinrich, Gross, Atan, Hajnoczky, Gyorgy, Hardwick, J Marie, Harris, Isaac S, Hengartner, Michael O, Hetz, Claudio, Ichijo, Hidenori, Jäättelä, Marja, Joseph, Bertrand, Jost, Philipp J, Juin, Philippe P, Kaiser, William J, Karin, Michael, Kaufmann, Thomas, Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N, Klionsky, Daniel J, Knight, Richard A, Kumar, Sharad, Lee, Sam W, Lemasters, John J, Levine, Beth, Linkermann, Andreas, Lipton, Stuart A, Lockshin, Richard A, López-Otín, Carlos, Lowe, Scott W, Luedde, Tom, Lugli, Enrico, MacFarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, Manic, Gwenola, Marine, Jean-Christophe, Martin, Seamus J, Martinou, Jean-Claude, Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Sonia, Miao, Edward A, Molkentin, Jeffery D, Moll, Ute M, Muñoz-Pinedo, Cristina, Nagata, Shigekazu, Nuñez, Gabriel, Oberst, Andrew, Oren, Moshe, Overholtzer, Michael, Pagano, Michele, Panaretakis, Theocharis, Pasparakis, Manolis, Penninger, Josef M, Pereira, David M, Pervaiz, Shazib, Peter, Marcus E, Piacentini, Mauro, Pinton, Paolo, Prehn, Jochen HM, Puthalakath, Hamsa, Rabinovich, Gabriel A, Rehm, Markus, Rizzuto, Rosario, Rodrigues, Cecilia MP, Rubinsztein, David C, Rudel, Thomas, Ryan, Kevin M, Sayan, Emre, Scorrano, Luca, Shao, Feng, Shi, Yufang, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stockwell, Brent R, Strasser, Andreas, Szabadkai, Gyorgy, Tait, Stephen WG, Tang, Daolin, Tavernarakis, Nektarios, Thorburn, Andrew, Tsujimoto, Yoshihide, Turk, Boris, Vanden Berghe, Tom, Vandenabeele, Peter, Vander Heiden, Matthew G, Villunger, Andreas, Virgin, Herbert W, Vousden, Karen H, Vucic, Domagoj, Wagner, Erwin F, Walczak, Henning, Wallach, David, Wang, Ying, Wells, James A, Wood, Will, Yuan, Junying, Zakeri, Zahra, Zhivotovsky, Boris, Zitvogel, Laurence, Melino, Gerry, and Kroemer, Guido

Subjects
Necrosis, Cell Death, Mitochondrial Permeability Transition Pore, Animals, Humans, Lysosomes, Mitochondrial Membrane Transport Proteins, 3. Good health
Abstract

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

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