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

Cell Death and Differentiation, Journal Year: 2018, Volume and Issue: 25(3), P. 486 - 541

Published: Jan. 23, 2018

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

Language: Английский

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Chloroquine inhibits autophagic flux by decreasing autophagosome-lysosome fusion

Autophagy, Journal Year: 2018, Volume and Issue: 14(8), P. 1435 - 1455

Published: June 26, 2018

Macroautophagy/autophagy is a conserved transport pathway where targeted structures are sequestered by phagophores, which mature into autophagosomes, and then delivered lysosomes for degradation. Autophagy involved in the pathophysiology of numerous diseases its modulation beneficial outcome specific diseases. Several lysosomal inhibitors such as bafilomycin A1 (BafA1), protease chloroquine (CQ), have been used interchangeably to block autophagy vitro experiments assuming that they all primarily Among them, only CQ derivate hydroxychloroquine (HCQ) FDA-approved drugs thus currently principal compounds clinical trials aimed treat tumors through inhibition. However, precise mechanism how blocks remains be firmly demonstrated. In this study, we focus on inhibits directly compare effects those BafA1. We show mainly impairing autophagosome fusion with rather than affecting acidity and/or degradative activity organelle. Furthermore, induces an autophagy-independent severe disorganization Golgi endo-lysosomal systems, might contribute impairment. Strikingly, HCQ-treated mice also kidney intestinal tissues. Altogether, our data reveal HCQ not bona fide surrogates other types late stage vivo experiments. Moreover, multiple cellular alterations caused call caution when interpreting results obtained blocking drug.

Language: Английский

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Molecular definitions of autophagy and related processes

The EMBO Journal, Journal Year: 2017, Volume and Issue: 36(13), P. 1811 - 1836

Published: June 8, 2017

Language: Английский

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Macrophages and Metabolism in the Tumor Microenvironment

Cell Metabolism, Journal Year: 2019, Volume and Issue: 30(1), P. 36 - 50

Published: July 1, 2019

Language: Английский

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Autophagy pathway: Cellular and molecular mechanisms

Autophagy, Journal Year: 2017, Volume and Issue: 14(2), P. 207 - 215

Published: Sept. 21, 2017

Macroautophagy/autophagy is an essential, conserved self-eating process that cells perform to allow degradation of intracellular components, including soluble proteins, aggregated organelles, macromolecular complexes, and foreign bodies. The requires formation a double-membrane structure containing the sequestered cytoplasmic material, autophagosome, ultimately fuses with lysosome. This review will define this cellular pathways required, from double membrane fusion lysosomes in molecular terms, particular highlight recent progress our understanding complex process.

Language: Английский

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Emerging functions of the EGFR in cancer

Molecular Oncology, Journal Year: 2017, Volume and Issue: 12(1), P. 3 - 20

Published: Nov. 10, 2017

The physiological function of the epidermal growth factor receptor ( EGFR ) is to regulate epithelial tissue development and homeostasis. In pathological settings, mostly in lung breast cancer glioblastoma, a driver tumorigenesis. Inappropriate activation mainly results from amplification point mutations at genomic locus , but transcriptional upregulation or ligand overproduction due autocrine/paracrine mechanisms has also been described. Moreover, increasingly recognized as biomarker resistance tumors, its secondary have found arise under drug pressure. This evidence, addition prominent that this plays normal epithelia, prompted intense investigations into role both level. Despite large body knowledge obtained over last two decades, previously unrecognized (herein defined ‘noncanonical’) functions are currently emerging. Here, we will initially review canonical ligand‐induced signaling pathway, with particular emphasis regulation by endocytosis subversion human tumors. We then focus on most recent advances uncovering noncanonical stress‐induced trafficking, autophagy, energy metabolism, perspective future therapeutic applications.

Language: Английский

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Autophagy in major human diseases

The EMBO Journal, Journal Year: 2021, Volume and Issue: 40(19)

Published: Aug. 30, 2021

Review30 August 2021Open Access Autophagy in major human diseases Daniel J Klionsky orcid.org/0000-0002-7828-8118 Life Sciences Institute, University of Michigan, Ann Arbor, MI, USA Search for more papers by this author Giulia Petroni Department Radiation Oncology, Weill Cornell Medical College, New York, NY, Ravi K Amaravadi Medicine, Pennsylvania, Philadelphia, PA, Abramson Cancer Center, Eric H Baehrecke Molecular, Cell and Biology, Massachusetts School, Worcester, MA, Andrea Ballabio orcid.org/0000-0003-1381-4604 Telethon Institute Genetics Pozzuoli, Italy Translational Sciences, Section Pediatrics, Federico II University, Naples, Molecular Human Genetics, Baylor College Jan Dan Duncan Neurological Research Texas Children Hospital, Houston, TX, Patricia Boya orcid.org/0000-0003-3045-951X Margarita Salas Center Biological Research, Spanish National Council, Madrid, Spain José Manuel Bravo-San Pedro Faculty Physiology, Complutense Networked Biomedical Neurodegenerative Diseases (CIBERNED), Ken Cadwell Kimmel Biology Medicine at the Skirball York Grossman School Microbiology, Division Gastroenterology Hepatology, Langone Health, Francesco Cecconi orcid.org/0000-0002-5614-4359 Stress Survival Unit, Autophagy, Recycling Disease (CARD), Danish Society Copenhagen, Denmark Pediatric Onco-Hematology Gene Therapy, IRCCS Bambino Gesù Children's Rome, Rome 'Tor Vergata', Augustine M Choi Pulmonary Critical Care Joan Sanford I. York-Presbyterian Mary E Nephrology Hypertension, Charleen T Chu orcid.org/0000-0002-5052-8271 Pathology, Pittsburgh Pittsburgh, Patrice Codogno orcid.org/0000-0002-5492-3180 Institut Necker-Enfants Malades, INSERM U1151-CNRS UMR 8253, Paris, France Université de Maria Isabel Colombo Laboratorio Mecanismos Moleculares Implicados en el Tráfico Vesicular y la Autofagia-Instituto Histología Embriología (IHEM)-Universidad Nacional Cuyo, CONICET- Facultad Ciencias Médicas, Mendoza, Argentina Ana Cuervo orcid.org/0000-0002-0771-700X Developmental Albert Einstein Bronx, Aging Studies, Vojo Deretic Inflammation Metabolism (AIM, Excellence, Mexico Health Albuquerque, NM, Ivan Dikic orcid.org/0000-0001-8156-9511 Biochemistry II, Goethe Frankfurt, Frankfurt am Main, Germany Buchmann Zvulun Elazar Biomolecular The Weizmann Science, Rehovot, Israel Eeva-Liisa Eskelinen Biomedicine, Turku, Finland Gian Fimia orcid.org/0000-0003-4438-3325 Sapienza Epidemiology, Preclinical Advanced Diagnostics, Infectious 'L. Spallanzani' IRCCS, David A Gewirtz orcid.org/0000-0003-0437-4934 Pharmacology Toxicology, Virginia Commonwealth Richmond, VA, Douglas R Green Immunology, St. Jude Memphis, TN, Malene Hansen Burnham Prebys Discovery Program Development, Aging, Regeneration, La Jolla, CA, Marja Jäättelä orcid.org/0000-0001-5950-7111 Death Metabolism, & Disease, Cellular Terje Johansen orcid.org/0000-0003-1451-9578 Group, Tromsø—The Arctic Norway, Tromsø, Norway Gábor Juhász Szeged, Hungary Anatomy, Eötvös Loránd Budapest, Vassiliki Karantza Merck Co., Inc., Kenilworth, NJ, Claudine Kraft orcid.org/0000-0002-3324-4701 ZBMZ, Freiburg, CIBSS - Centre Integrative Signalling Guido Kroemer orcid.org/0000-0002-9334-4405 Recherche des Cordeliers, Equipe Labellisée par Ligue Contre le Cancer, Sorbonne Université, Inserm U1138, Universitaire France, Metabolomics Platforms, Gustave Roussy, Villejuif, Pôle Biologie, Hôpital Européen Georges Pompidou, AP-HP, Suzhou Systems Chinese Academy Suzhou, China Karolinska Women's Stockholm, Sweden Nicholas Ktistakis Programme, Babraham Cambridge, UK Sharad Kumar orcid.org/0000-0001-7126-9814 South Australia, Adelaide, SA, Australia Carlos Lopez-Otin orcid.org/0000-0001-6964-1904 Departamento Bioquímica Biología Medicina, Instituto Universitario Oncología del Principado Asturias (IUOPA), Universidad Oviedo, Centro Investigación Biomédica Red Cáncer (CIBERONC), Kay F Macleod Ben May Gordon W-338, Chicago, IL, Frank Madeo Biosciences, NAWI Graz, Austria BioTechMed-Graz, Field Excellence BioHealth – Jennifer Martinez Immunity, Laboratory, Environmental NIH, Triangle Park, NC, Alicia Meléndez Department, Queens City Flushing, Graduate PhD Programs Noboru Mizushima orcid.org/0000-0002-6258-6444 Tokyo, Japan Christian Münz orcid.org/0000-0001-6419-1940 Viral Immunobiology, Experimental Zurich, Switzerland Josef Penninger Biotechnology Austrian (IMBA), Vienna BioCenter (VBC), Vienna, British Columbia, Vancouver, BC, Canada Rushika Perera orcid.org/0000-0003-2435-2273 California, San Francisco, Helen Diller Family Comprehensive Mauro Piacentini orcid.org/0000-0003-2919-1296 "Tor Vergata", Laboratory Cytology Russian Saint Petersburg, Russia Fulvio Reggiori orcid.org/0000-0003-2652-2686 Cells Systems, Section, Groningen, Netherlands C Rubinsztein Cambridge Dementia Kevin Ryan Beatson Glasgow, Junichi Sadoshima Cardiovascular Rutgers Jersey Newark, Laura Santambrogio Sandra Edward Meyer Caryl Englander Precision Luca Scorrano orcid.org/0000-0002-8515-8928 Istituto Veneto di Medicina Molecolare, Padova, Hans-Uwe Simon Pharmacology, Bern, Clinical Immunology Allergology, Sechenov Moscow, Fundamental Kazan Federal Kazan, Anna Katharina Kennedy Rheumatology, NDORMS, Oxford, Anne Simonsen orcid.org/0000-0003-4711-7057 Basic Oslo, Reprogramming, Oslo Hospital Montebello, Alexandra Stolz orcid.org/0000-0002-3340-439X Nektarios Tavernarakis orcid.org/0000-0002-5253-1466 Biotechnology, Foundation Technology-Hellas, Heraklion, Crete, Greece Sharon Tooze orcid.org/0000-0002-2182-3116 Francis Crick London, Tamotsu Yoshimori orcid.org/0000-0001-9787-3788 Osaka Suita, Intracellular Membrane Dynamics, Frontier Integrated Science Division, Open Transdisciplinary Initiatives (OTRI), Junying Yuan Interdisciplinary on Chemistry, Shanghai Organic Shanghai, Harvard Boston, Zhenyu Yue Neurology, Friedman Brain Icahn Mount Sinai, Qing Zhong orcid.org/0000-0001-6979-955X Key Differentiation Apoptosis Ministry Education, Pathophysiology, Jiao Tong (SJTU-SM), Lorenzo Galluzzi Corresponding Author [email protected] orcid.org/0000-0003-2257-8500 Dermatology, Yale Haven, CT, Pietrocola orcid.org/0000-0002-2930-234X Biosciences Nutrition, Huddinge, mor

Language: Английский

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The coming of age of chaperone-mediated autophagy

Nature Reviews Molecular Cell Biology, Journal Year: 2018, Volume and Issue: 19(6), P. 365 - 381

Published: April 6, 2018

Language: Английский

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Mitochondrial metabolism and cancer

Cell Research, Journal Year: 2017, Volume and Issue: 28(3), P. 265 - 280

Published: Dec. 8, 2017

Glycolysis has long been considered as the major metabolic process for energy production and anabolic growth in cancer cells. Although such a view instrumental development of powerful imaging tools that are still used clinics, it is now clear mitochondria play key role oncogenesis. Besides exerting central bioenergetic functions, provide indeed building blocks tumor anabolism, control redox calcium homeostasis, participate transcriptional regulation, govern cell death. Thus, constitute promising targets novel anticancer agents. However, tumors arise, progress, respond to therapy context an intimate crosstalk with host immune system, many immunological functions rely on intact mitochondrial metabolism. Here, we review cell-intrinsic cell-extrinsic mechanisms through which influence all steps oncogenesis, focus therapeutic potential targeting metabolism therapy.

Language: Английский

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Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States

Cell Metabolism, Journal Year: 2018, Volume and Issue: 27(6), P. 1176 - 1199

Published: June 1, 2018

Language: Английский

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