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

Cell Death and Differentiation, Год журнала: 2018, Номер 25(3), С. 486 - 541

Опубликована: Янв. 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.

Язык: Английский

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Immunogenic cell death in cancer and infectious disease

Nature reviews. Immunology, Год журнала: 2016, Номер 17(2), С. 97 - 111

Опубликована: Окт. 17, 2016

Язык: Английский

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The molecular machinery of regulated cell death

Cell Research, Год журнала: 2019, Номер 29(5), С. 347 - 364

Опубликована: Апрель 4, 2019

Cells may die from accidental cell death (ACD) or regulated (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 have been identified are increasingly being implicated in various human pathologies. Here, we critically review the current state art regarding types RCD, including necroptosis, pyroptosis, ferroptosis, entotic death, netotic parthanatos, lysosome-dependent autophagy-dependent alkaliptosis oxeiptosis. The in-depth comprehension each these lethal subroutines their intercellular consequences uncover therapeutic targets for avoidance pathogenic loss.

Язык: Английский

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Mitochondrial metabolism and cancer

Cell Research, Год журнала: 2017, Номер 28(3), С. 265 - 280

Опубликована: Дек. 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.

Язык: Английский

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Guidelines for the use of flow cytometry and cell sorting in immunological studies (second edition)

European Journal of Immunology, Год журнала: 2019, Номер 49(10), С. 1457 - 1973

Опубликована: Окт. 1, 2019

These guidelines are a consensus work of considerable number members the immunology and flow cytometry community. They provide theory key practical aspects enabling immunologists to avoid common errors that often undermine immunological data. Notably, there comprehensive sections all major immune cell types with helpful Tables detailing phenotypes in murine human cells. The latest techniques applications also described, featuring examples data can be generated and, importantly, how analysed. Furthermore, tips, tricks pitfalls avoid, written peer-reviewed by leading experts field, making this an essential research companion.

Язык: Английский

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Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy

Signal Transduction and Targeted Therapy, Год журнала: 2022, Номер 7(1)

Опубликована: Июнь 20, 2022

Abstract In recent years, immunotherapy represented by immune checkpoint inhibitors (ICIs) has led to unprecedented breakthroughs in cancer treatment. However, the fact that many tumors respond poorly or even not ICIs, partly caused absence of tumor-infiltrating lymphocytes (TILs), significantly limits application ICIs. Converting these “cold” into “hot” may ICIs is an unsolved question immunotherapy. Since it a general characteristic cancers resist apoptosis, induction non-apoptotic regulated cell death (RCD) emerging as new treatment strategy. Recently, several studies have revealed interaction between RCD and antitumor immunity. Specifically, autophagy, ferroptosis, pyroptosis, necroptosis exhibit synergistic responses while possibly exerting inhibitory effects on responses. Thus, targeted therapies (inducers inhibitors) against combination with exert potent activity, resistant This review summarizes multilevel relationship immunity RCD, including necroptosis, potential targeting improve efficacy malignancy.

Язык: Английский

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Mitochondrial complex I inhibition triggers a mitophagy-dependent ROS increase leading to necroptosis and ferroptosis in melanoma cells

Cell Death and Disease, Год журнала: 2017, Номер 8(3), С. e2716 - e2716

Опубликована: Март 30, 2017

Inhibition of complex I (CI) the mitochondrial respiratory chain by BAY 87-2243 ('BAY') triggers death BRAFV600E melanoma cell lines and inhibits in vivo tumor growth. Here we studied mechanism which this inhibition induces death. treatment depolarized membrane potential (Δψ), increased cellular ROS levels, stimulated lipid peroxidation reduced glutathione levels. These effects were paralleled opening permeability transition pore (mPTP) stimulation autophagosome formation mitophagy. BAY-induced was not due to glucose shortage inhibited antioxidant α-tocopherol mPTP inhibitor cyclosporin A. Tumor necrosis factor receptor-associated protein 1 (TRAP1) overexpression BAY-treated cells lowered levels death, whereas latter potentiated TRAP1 knockdown. Knockdown autophagy-related 5 (ATG5) BAY-stimulated formation, increase phosphatase tensin homolog-induced putative kinase (PINK1) Δψ depolarization, mitophagy stimulation, Dynamin-related (Drp1) knockdown induced filamentation The insensitive pancaspase z-VAD-FMK, but necroptosis inhibitors (necrostatin-1, necrostatin-1s)) key proteins (receptor-interacting serine/threonine-protein (RIPK1) mixed lineage domain-like (MLKL)). also ferroptosis ferrostatin-1 ferroptosis-inhibiting peroxidase 4 (GPX4). This peroxidation. Conversely, GPX4 We propose a events which: (i) CI that (ii) stimulate an associated increase, leading (iii) activation combined necroptotic/ferroptotic

Язык: Английский

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Iron homeostasis and iron-regulated ROS in cell death, senescence and human diseases

Biochimica et Biophysica Acta (BBA) - General Subjects, Год журнала: 2019, Номер 1863(9), С. 1398 - 1409

Опубликована: Июнь 20, 2019

Язык: Английский

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Linking cellular stress responses to systemic homeostasis

Nature Reviews Molecular Cell Biology, Год журнала: 2018, Номер 19(11), С. 731 - 745

Опубликована: Окт. 10, 2018

Язык: Английский

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Microglia-derived TNF-α mediates endothelial necroptosis aggravating blood brain–barrier disruption after ischemic stroke

Cell Death and Disease, Год журнала: 2019, Номер 10(7)

Опубликована: Июнь 20, 2019

Abstract Endothelium (EC) is a key component of blood–brain barrier (BBB), and has an important position in the neurovascular unit. Its dysfunction death after cerebral ischemic/reperfusion (I/R) injury not only promote evolution neuroinflammation brain edema, but also increase risk intracerebral hemorrhage thrombolytic therapies. However, mechanism specific interventions EC I/R are poorly understood. Here we showed that necroptosis was underlying death, which promoted BBB breakdown injury. Treatment rats with receptor interacting protein kinase 1 (RIPK1)-inhibitor, necrostatin-1 reduced endothelial leakage. We furthermore perivascular M1-like microglia-induced leading to disruption requires tumor necrosis factor-α (TNF-α) secreted by M1 type microglia its receptor, TNF (TNFR1), on endothelium as primary mediators these effects. More importantly, anti-TNFα (infliximab, potent clinically used drug) treatment significantly ameliorate necroptosis, destruction improve stroke outcomes. Our data identify previously unexplored role for suggest infliximab might serve potential drug therapy.

Язык: Английский

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