Log in

Relevant bibliographies by topics / Cell death pathways / Journal articles

To see the other types of publications on this topic, follow the link: Cell death pathways.

Journal articles on the topic 'Cell death pathways'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Cell death pathways.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Fernández-Lázaro, Diego, César Ignacio Fernández-Lázaro, and Martínez Alfredo Córdova. "Cell Death: Mechanisms and Pathways in Cancer Cells." Cancer Medicine Journal 1, no. 1 (August 31, 2018): 12–23. http://dx.doi.org/10.46619/cmj.2018.1-1003.

Full text

Abstract:

Programmed cell death is an essential physiological and biological process for the proper development and functioning of the organism. Apoptosis is the term that describes the most frequent form of programmed cell death and derives from the morphological characteristics of this type of death caused by cellular suicide. Apoptosis is highly regulated to maintain homeostasis in the body, since its imbalances by increasing and decreasing lead to different types of diseases. In this review, we aim to describe the mechanisms of cell death and the pathways through apoptosis is initiated, transmitted, regulated, and executed.

APA, Harvard, Vancouver, ISO, and other styles

2

Stekovic, Slaven, and Frank Madeo. "Cell death pathways." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1833, no. 12 (December 2013): 3447. http://dx.doi.org/10.1016/j.bbamcr.2013.09.016.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Fulda, Simone. "Alternative Cell Death Pathways and Cell Metabolism." International Journal of Cell Biology 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/463637.

Full text

Abstract:

While necroptosis has for long been viewed as an accidental mode of cell death triggered by physical or chemical damage, it has become clear over the last years that necroptosis can also represent a programmed form of cell death in mammalian cells. Key discoveries in the field of cell death research, including the identification of critical components of the necroptotic machinery, led to a revised concept of cell death signaling programs. Several regulatory check and balances are in place in order to ensure that necroptosis is tightly controlled according to environmental cues and cellular needs. This network of regulatory mechanisms includes metabolic pathways, especially those linked to mitochondrial signaling events. A better understanding of these signal transduction mechanisms will likely contribute to open new avenues to exploit our knowledge on the regulation of necroptosis signaling for therapeutic application in the treatment of human diseases.

APA, Harvard, Vancouver, ISO, and other styles

4

Choi, Soo Youn, Whaseon Lee-Kwon, Hwan Hee Lee, Jun Ho Lee, Satoru Sanada, and Hyug Moo Kwon. "Multiple cell death pathways are independently activated by lethal hypertonicity in renal epithelial cells." American Journal of Physiology-Cell Physiology 305, no. 10 (November 15, 2013): C1011—C1020. http://dx.doi.org/10.1152/ajpcell.00384.2012.

Full text

Abstract:

When hypertonicity is imposed with sufficient intensity and acuteness, cells die. Here we investigated the cellular pathways involved in death using a cell line derived from renal epithelium. We found that hypertonicity rapidly induced activation of an intrinsic cell death pathway—release of cytochrome c and activation of caspase-3 and caspase-9—and an extrinsic pathway—activation of caspase-8. Likewise, a lysosomal pathway of cell death characterized by partial lysosomal rupture and release of cathepsin B from lysosomes to the cytosol was also activated. Relationships among the pathways were examined using specific inhibitors. Caspase inhibitors did not affect cathepsin B release into the cytosol by hypertonicity. In addition, cathepsin B inhibitors and caspase inhibitors did not affect hypertonicity-induced cytochrome c release, suggesting that the three pathways were independently activated. Combined inhibition of caspases and cathepsin B conferred significantly more protection from hypertonicity-induced cell death than inhibition of caspase or cathepsin B alone, indicating that all the three pathways contributed to the hypertonicity-induced cell death. Similar pattern of sensitivity to the inhibitors was observed in two other cell lines derived from renal epithelia. We conclude that multiple cell death pathways are independently activated early in response to lethal hypertonic stress in renal epithelial cells.

APA, Harvard, Vancouver, ISO, and other styles

5

Shymanskyy, I. O., O. O. Lisakovska, A. O. Mazanova, D. O. Labudzynskyi, A. V. Khomenko, and M. M. Veliky. "Prednisolone and vitamin D(3) modulate oxidative metabolism and cell death pathways in blood and bone marrow mononuclear cells." Ukrainian Biochemical Journal 88, no. 5 (October 31, 2016): 38–47. http://dx.doi.org/10.15407/ubj88.05.038.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Wong, Brian, and Yongwon Choi. "Pathways leading to cell death in T cells." Current Opinion in Immunology 9, no. 3 (June 1997): 358–64. http://dx.doi.org/10.1016/s0952-7915(97)80082-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Mansilla, Sylvia, Laia Llovera, and Jose Portugal. "Chemotherapeutic Targeting of Cell Death Pathways." Anti-Cancer Agents in Medicinal Chemistry 12, no. 3 (March 1, 2012): 226–38. http://dx.doi.org/10.2174/187152012800228805.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Jin, Zhaoyu, and Wafik S. El-Deiry. "Overview of cell death signaling pathways." Cancer Biology & Therapy 4, no. 2 (February 2, 2005): 147–71. http://dx.doi.org/10.4161/cbt.4.2.1508.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Horowitz, Stuart. "Pathways to Cell Death in Hyperoxia." Chest 116 (July 1999): 64S—67S. http://dx.doi.org/10.1378/chest.116.suppl_1.64s.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

MacFarlane, M. "Cell death pathways – potential therapeutic targets." Xenobiotica 39, no. 8 (July 21, 2009): 616–24. http://dx.doi.org/10.1080/00498250903137990.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Golstein, Pierre, and Guido Kroemer. "A multiplicity of cell death pathways." EMBO reports 8, no. 9 (July 27, 2007): 829–33. http://dx.doi.org/10.1038/sj.embor.7401042.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Piacentini, M., and G. Kroemer. "Cell death pathways in retroviral infection." Cell Death & Differentiation 12, S1 (June 27, 2005): 835–36. http://dx.doi.org/10.1038/sj.cdd.4401655.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

A Ali Azzwali, Abdu-Alhameed, and Azab Elsayed Azab. "Mechanisms of programmed cell death." Journal of Applied Biotechnology & Bioengineering 6, no. 4 (July 10, 2019): 156–58. http://dx.doi.org/10.15406/jabb.2019.06.00188.

Full text

Abstract:

The present review aims to spotlight on the mechanisms and stages of programmed cell death. Apoptosis, known as programmed cell death, is a homeostatic mechanism that generally occurs during development and aging in order to keep cells in tissue. It can also act as a protective mechanism, for example, in immune response or if cells are damaged by toxin agents or diseases. In cancer treatment, drugs and irradiation used in chemotherapy leads to DNA damage, which results in triggering apoptosis through the p53 dependent pathway in cancer treatment, drugs and irradiation used in chemotherapy leads to DNA damage, which results in triggering apoptosis through the p53 dependent pathway. Corticosteroids can cause apoptotic death in a number of cells. A number of changes in cell morphology are related to the different stages of apoptosis, which includes nuclear DNA fragmentation, cell shrinkage, chromatin condensation, membrane blebbing, and the formation of apoptotic bodies. There are three pathways for apoptosis, the intrinsic (mitochondrial) and extrinsic (death receptor) are the two major paths that are interlinked and that can effect one another. Conclusion: It can be concluded that apoptosis is a homeostatic mechanism that generally occurs during development and aging in order to keep cells in tissue. Drugs and irradiation used in chemotherapy leads to DNA damage, which results in triggering apoptosis through the p53 dependent pathway. The apoptosis, stages are includes nuclear DNA fragmentation, cell shrinkage, chromatin condensation, membrane blebbing, and the formation of apoptotic bodies. There are three pathways for apoptosis.

APA, Harvard, Vancouver, ISO, and other styles

14

Kerr, Shannic-Le, Cynthia Mathew, and Reena Ghildyal. "Rhinovirus and Cell Death." Viruses 13, no. 4 (April 7, 2021): 629. http://dx.doi.org/10.3390/v13040629.

Full text

Abstract:

Rhinoviruses (RVs) are the etiological agents of upper respiratory tract infections, particularly the common cold. Infections in the lower respiratory tract is shown to cause severe disease and exacerbations in asthma and COPD patients. Viruses being obligate parasites, hijack host cell pathways such as programmed cell death to suppress host antiviral responses and prolong viral replication and propagation. RVs are non-enveloped positive sense RNA viruses with a lifecycle fully contained within the cytoplasm. Despite decades of study, the details of how RVs exit the infected cell are still unclear. There are some diverse studies that suggest a possible role for programmed cell death. In this review, we aimed to consolidate current literature on the impact of RVs on cell death to inform future research on the topic. We searched peer reviewed English language literature in the past 21 years for studies on the interaction with and modulation of cell death pathways by RVs, placing it in the context of the broader knowledge of these interconnected pathways from other systems. Our review strongly suggests a role for necroptosis and/or autophagy in RV release, with the caveat that all the literature is based on RV-A and RV-B strains, with no studies to date examining the interaction of RV-C strains with cell death pathways.

APA, Harvard, Vancouver, ISO, and other styles

15

Bermpohl, Daniela, Annett Halle, Dorette Freyer, Emilie Dagand, Johann S. Braun, Ingo Bechmann, Nicolas W. J. Schröder, and Joerg R. Weber. "Bacterial programmed cell death of cerebral endothelial cells involves dual death pathways." Journal of Clinical Investigation 115, no. 6 (June 1, 2005): 1607–15. http://dx.doi.org/10.1172/jci23223.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

de Vries, J. F., P. A. von dem Borne, M. H. M. Heemskerk, R. Willemze, J. H. F. Falkenburg, and R. M. Y. Barge. "Retroviral Interference with Execution Pathways in Target Cells To Unravel Mechanisms of Cytotoxic T Cell-Mediated Cell Death." Blood 104, no. 11 (November 16, 2004): 1267. http://dx.doi.org/10.1182/blood.v104.11.1267.1267.

Full text

Abstract:

Abstract Cytotoxic T lymphocytes (CTLs) mediate target cell death by different effector mechanisms. We investigated whether a correlation exists between the kinetics of CTL-induced killing of the target cell and the different apoptotic pathways executed by the CTL. Different CTL clones were isolated using from a patient with CML after receiving donor lymphocyte infusions from an HLA-identical donor. These CTL clones recognized minor antigens expressed on the EBV-LCL cells from the patient. Since these clones were not all equally effective in killing the same target cells, we hypothesized that these T cells may induce different apoptotic pathways. In order to study the different execution pathways in the target cell, we generated retroviral constructs encoding the anti-apoptotic genes FADD-DN and FLIP, both inhibiting death receptor-mediated killing, and the granzyme B (GrB)-inhibitor PI-9. Using a retroviral delivery system, these constructs were transduced to the EBV-LCL cells. The cells highly overexpressing the gene of interest were sorted based on coexpression of a reporter gene, which was confirmed by Western Blot analysis. Both the wildtype (EBV-WT) and the transduced EBV cells (EBV-FADD-DN, EBV-FLIP and EBV-PI-9) were used as targets and the different CTL clones as effectors (E:T ratio = 1:1) in a quantitative CFSE-based cytotoxicity assay using Flow-Count Fluorospheres. To analyze the mechanism of immediate cell death caused by rapidly killing CTL clones, EBV-WT cells were exposed for 2 hours (h) to these clones, resulting in 30% lysis. This lysis could neither be blocked by FADD-DN or FLIP, nor by PI-9. Furthermore, no inhibition was obtained using the general caspase-inhibitor z-VAD-FMK, indicating that the killing was caspase-independent. In agreement with this observation, specific triggering of the Fas receptor pathway by an agonistic Fas antibody (100 ng/ml) did not induce any apoptosis within 2 h. To study CTL-induced cell death after a longer period, we analyzed CTL clones with different rates of killing and measured cytotoxicity after 5 and 24 h. Rapidly killing clones induced 60–70% cell death of the EBV-WT within 5 h, whereas slowly killing CTL clones did not show cytotoxicity after 5 h, but induced 50–60% cell death of EBV-WT after 24 h of incubation. Inhibition of CTL-mediated cell death by overexpression of the different anti-apoptotic proteins was comparable for all types of clones, showing 10–35% inhibition by either FADD-DN or FLIP and 20–55% by PI-9, indicating that both pathways are involved. As control, Fas antibody-induced apoptosis was almost completely inhibited in EBV-FADD-DN and EBV-FLIP, demonstrating highly effective block of the Fas-receptor pathway by these constructs. These results indicate that despite different kinetics of killing, all T cell clones used both the death receptor pathway and GrB release to kill its targets. In conclusion: 1. Interference with the Fas receptor or the GrB effector pathway cannot prevent CTL-mediated target cell death within the first 2 h of exposure, indicating that this lysis is probably directly perforin-mediated. 2. Both slowly and rapidly killing CTL clones use various effector mechanisms to kill their target cells, including both the death receptor and GrB pathways. In case of slower mediated cell death, not the execution pathway induced by the CTL, but affinity between TCR and MHC/peptide complex and other effector/target interactions more likely determine the kinetics of CTL-mediated cell death.

APA, Harvard, Vancouver, ISO, and other styles

17

Wahyunitisari, ManikRetno, NiMade Mertaniasih, Muhammad Amin, WayanT Artama, and EkoB Koendhori. "Vitamin D, cell death pathways, and tuberculosis." International Journal of Mycobacteriology 6, no. 4 (2017): 349. http://dx.doi.org/10.4103/ijmy.ijmy_120_17.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Scott, Iain, and David C. Logan. "Mitochondria and cell death pathways in plants." Plant Signaling & Behavior 3, no. 7 (July 2008): 475–77. http://dx.doi.org/10.4161/psb.3.7.5678.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Philpott, Karen, and Laura Facci. "MAP Kinase Pathways in Neuronal Cell Death." CNS & Neurological Disorders - Drug Targets 7, no. 1 (February 1, 2008): 83–97. http://dx.doi.org/10.2174/187152708783885129.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Ricci, M. Stacey, and Wei‐Xing Zong. "Chemotherapeutic Approaches for Targeting Cell Death Pathways." Oncologist 11, no. 4 (April 2006): 342–57. http://dx.doi.org/10.1634/theoncologist.11-4-342.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Duprez, Linde, Ellen Wirawan, Tom Vanden Berghe, and Peter Vandenabeele. "Major cell death pathways at a glance." Microbes and Infection 11, no. 13 (November 2009): 1050–62. http://dx.doi.org/10.1016/j.micinf.2009.08.013.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Vandenabeele, P., T. Vanden Berghe, and N. Festjens. "Caspase Inhibitors Promote Alternative Cell Death Pathways." Science's STKE 2006, no. 358 (October 17, 2006): pe44. http://dx.doi.org/10.1126/stke.3582006pe44.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Ferri, Karine F., and Guido Kroemer. "Organelle-specific initiation of cell death pathways." Nature Cell Biology 3, no. 11 (November 2001): E255—E263. http://dx.doi.org/10.1038/ncb1101-e255.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Perlson, Eran, Sandra Maday, Meng-meng Fu, Armen J. Moughamian, and Erika L. F. Holzbaur. "Retrograde axonal transport: pathways to cell death?" Trends in Neurosciences 33, no. 7 (July 2010): 335–44. http://dx.doi.org/10.1016/j.tins.2010.03.006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Nakayama, Masafumi, Kazumi Ishidoh, Nobuhiko Kayagaki, Yuko Kojima, Noriko Yamaguchi, Hiroyasu Nakano, Eiki Kominami, Ko Okumura, and Hideo Yagita. "Multiple Pathways of TWEAK-Induced Cell Death." Journal of Immunology 168, no. 2 (January 15, 2002): 734–43. http://dx.doi.org/10.4049/jimmunol.168.2.734.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Salvesen, G. "ID: 152 Proteolytic pathways in cell death." Journal of Thrombosis and Haemostasis 4, s1 (October 2006): 26. http://dx.doi.org/10.1111/j.1538-7836.2006.00152.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Peterson, Jeanne S., B. Paige Bass, Deborah Jue, Antony Rodriguez, John M. Abrams, and Kimberly McCall. "Noncanonical cell death pathways act duringDrosophila oogenesis." genesis 45, no. 6 (2007): 396–404. http://dx.doi.org/10.1002/dvg.20306.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Zhang, Zhengguo, Ming Wang, Florian Eisel, Svetlin Tchatalbachev, Trinad Chakraborty, Andreas Meinhardt, and Sudhanshu Bhushan. "UropathogenicEscherichia coliEpigenetically Manipulate Host Cell Death Pathways." Journal of Infectious Diseases 213, no. 7 (November 29, 2015): 1198–207. http://dx.doi.org/10.1093/infdis/jiv569.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Zlotorynski, Eytan. "At the crossroads of cell death pathways." Nature Reviews Molecular Cell Biology 15, no. 4 (March 21, 2014): 222. http://dx.doi.org/10.1038/nrm3782.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Hardwick, J. Marie, and Wen-Chih Cheng. "Mitochondrial Programmed Cell Death Pathways in Yeast." Developmental Cell 7, no. 5 (November 2004): 630–32. http://dx.doi.org/10.1016/j.devcel.2004.10.013.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Peixoto, Milena Simões, Marcos Felipe de Oliveira Galvão, and Silvia Regina Batistuzzo de Medeiros. "Cell death pathways of particulate matter toxicity." Chemosphere 188 (December 2017): 32–48. http://dx.doi.org/10.1016/j.chemosphere.2017.08.076.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Persaud-Sawin, D. A., and R.-M. N. Boustany. "Cell death pathways in juvenile Batten disease." Apoptosis 10, no. 5 (October 2005): 973–85. http://dx.doi.org/10.1007/s10495-005-0733-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Depraetere, Valérie, and Pierre Golstein. "Fas and other cell death signaling pathways." Seminars in Immunology 9, no. 2 (April 1997): 93–107. http://dx.doi.org/10.1006/smim.1997.0062.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Miyata, Tatsunori, and Laura E. Nagy. "Programmed cell death in alcohol-associated liver disease." Clinical and Molecular Hepatology 26, no. 4 (October 1, 2020): 618–25. http://dx.doi.org/10.3350/cmh.2020.0142.

Full text

Abstract:

Alcohol-associated liver disease (ALD), which ranges from mild disease to alcohol-associated hepatitis and cirrhosis, is the most prevalent type of chronic liver disease and a leading cause of morbidity and mortality worldwide. Accumulating evidence reveals that programmed cell death (PCD) plays a crucial role in progression of ALD involving crosstalk between hepatocytes and immune cells. Multiple pathways of PCD, including apoptosis, necroptosis, autophagy, pyroptosis and ferroptosis, are reported in ALD. Interestingly, PCD pathways are intimately linked and interdependent, making it difficult to therapeutically target a single pathway. This review clarifies the multiple types of PCD occurring in liver and focuses on crosstalk between hepatocytes and innate immune cells in ALD.

APA, Harvard, Vancouver, ISO, and other styles

35

Parsons, Melissa J., and Douglas R. Green. "Mitochondria in cell death." Essays in Biochemistry 47 (June 14, 2010): 99–114. http://dx.doi.org/10.1042/bse0470099.

Full text

Abstract:

Apoptosis can be thought of as a signalling cascade that results in the death of the cell. Properly executed apoptosis is critically important for both development and homoeostasis of most animals. Accordingly, defects in apoptosis can contribute to the development of autoimmune disorders, neurological diseases and cancer. Broadly speaking, there are two main pathways by which a cell can engage apoptosis: the extrinsic apoptotic pathway and the intrinsic apoptotic pathway. At the centre of the intrinsic apoptotic signalling pathway lies the mitochondrion, which, in addition to its role as the bioenergetic centre of the cell, is also the cell’s reservoir of pro-death factors which reside in the mitochondrial IMS (intermembrane space). During intrinsic apoptosis, pores are formed in the OMM (outer mitochondrial membrane) of the mitochondria in a process termed MOMP (mitochondrial outer membrane permeabilization). This allows for the release of IMS proteins; once released during MOMP, some IMS proteins, notably cytochrome c and Smac/DIABLO (Second mitochondria-derived activator of caspase/direct inhibitor of apoptosis-binding protein with low pI), promote caspase activation and subsequent cleavage of structural and regulatory proteins in the cytoplasm and the nucleus, leading to the demise of the cell. MOMP is achieved through the co-ordinated actions of pro-apoptotic members and inhibited by anti-apoptotic members of the Bcl-2 family of proteins. Other aspects of mitochondrial physiology, such as mitochondrial bioenergetics and dynamics, are also involved in processes of cell death that proceed through the mitochondria. Proper regulation of these mitochondrial functions is vitally important for the life and death of the cell and for the organism as a whole.

APA, Harvard, Vancouver, ISO, and other styles

36

Wang, Man, Shuai Jiang, Yinfeng Zhang, Peifeng Li, and Kun Wang. "The Multifaceted Roles of Pyroptotic Cell Death Pathways in Cancer." Cancers 11, no. 9 (September 5, 2019): 1313. http://dx.doi.org/10.3390/cancers11091313.

Full text

Abstract:

Cancer is a category of diseases involving abnormal cell growth with the potential to invade other parts of the body. Chemotherapy is the most widely used first-line treatment for multiple forms of cancer. Chemotherapeutic agents act via targeting the cellular apoptotic pathway. However, cancer cells usually acquire chemoresistance, leading to poor outcomes in cancer patients. For that reason, it is imperative to discover other cell death pathways for improved cancer intervention. Pyroptosis is a new form of programmed cell death that commonly occurs upon pathogen invasion. Pyroptosis is marked by cell swelling and plasma membrane rupture, which results in the release of cytosolic contents into the extracellular space. Currently, pyroptosis is proposed to be an alternative mode of cell death in cancer treatment. Accumulating evidence shows that the key components of pyroptotic cell death pathways, including inflammasomes, gasdermins and pro-inflammatory cytokines, are involved in the initiation and progression of cancer. Interfering with pyroptotic cell death pathways may represent a promising therapeutic option for cancer management. In this review, we describe the current knowledge regarding the biological significance of pyroptotic cell death pathways in cancer pathogenesis and also discuss their potential therapeutic utility.

APA, Harvard, Vancouver, ISO, and other styles

37

Henshall, D. C. "Apoptosis signalling pathways in seizure-induced neuronal death and epilepsy." Biochemical Society Transactions 35, no. 2 (March 20, 2007): 421–23. http://dx.doi.org/10.1042/bst0350421.

Full text

Abstract:

Delineating the molecular pathways underlying seizure-induced neuronal death may yield novel strategies for brain protection against prolonged or repetitive seizures. Glutamate-mediated excitotoxicity and necrosis is a primary contributing mechanism but seizures also activate programmed (apoptotic) cell death pathways. Apoptosis signalling pathways are typically initiated following perturbation of intracellular organelle function (intrinsic pathway) or by activated cell-surface-expressed death receptors (extrinsic pathway), with signalling cascades orchestrated in part by the Bcl-2 and caspase gene families. In this review, evidence for these pathways from experimental seizure modelling and clinical material from patients with intractable temporal lobe epilepsy is examined. Seizures cause mitochondrial dysfunction and activate intrinsic pathway components including pro-apoptotic Bcl-2 family proteins and caspases, processes that may be partly calcium-induced. The ER (endoplasmic reticulum) has emerged as a major intrinsic pathway trigger for apoptosis and its function may also be compromised following seizures and in epilepsy. The extrinsic, death-receptor-dependent pathway is also rapidly engaged following experimental seizures and in patient brain, supporting a previously unexpected apical role for a calcium-independent pathway. When considered alongside emerging functions of apoptosis-regulatory proteins in non-cell-death processes, including regulating intracellular calcium release and neuronal (re)structuring, apoptosis signalling pathways can be viewed as an important developing focus of research into how to obviate the deleterious impact of seizures on the brain.

APA, Harvard, Vancouver, ISO, and other styles

38

Chowdhury, Dipanjan, and Judy Lieberman. "Death by a Thousand Cuts: Granzyme Pathways of Programmed Cell Death." Annual Review of Immunology 26, no. 1 (April 2008): 389–420. http://dx.doi.org/10.1146/annurev.immunol.26.021607.090404.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

LEE, E. C. Y., and M. TENNISWOOD. "PROGRAMMED CELL DEATH AND SURVIVAL PATHWAYS IN PROSTATE CANCER CELLS." Archives of Andrology 50, no. 1 (January 2004): 27–32. http://dx.doi.org/10.1080/01485010490250498.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Hay, Stewart, and George Kannourakis. "A time to kill: viral manipulation of the cell death program." Journal of General Virology 83, no. 7 (July 1, 2002): 1547–64. http://dx.doi.org/10.1099/0022-1317-83-7-1547.

Full text

Abstract:

Many viruses have as part of their arsenal the ability to modulate the apoptotic pathways of the host. It is counter-intuitive that such simple organisms would be efficient at regulating this the most crucial pathway within the host, given the relative complexity of the host cells. Yet, viruses have the potential to initiate or stay the onset of programmed cell death through the manipulation of a variety of key apoptotic proteins. It is the intention of this review to provide an overview of viral gene products that are able to promote or inhibit apoptotic death of the host cell and to discuss their mechanisms of action. It is not until recently that the depth at which viruses exploit the apoptotic pathways of their host has been seen. This understanding may provide a great opportunity for future therapeutic ventures.

APA, Harvard, Vancouver, ISO, and other styles

41

Nakajima, H., P. Golstein, and P. A. Henkart. "The target cell nucleus is not required for cell-mediated granzyme- or Fas-based cytotoxicity." Journal of Experimental Medicine 181, no. 5 (May 1, 1995): 1905–9. http://dx.doi.org/10.1084/jem.181.5.1905.

Full text

Abstract:

The requirement for target cell nuclei in the two apoptotic death pathways used by cytotoxic lymphocytes was tested using model effector systems in which the granzyme and Fas pathways of target damage are isolated. Mast cell tumors expressing granzymes A and B in addition to cytolysin/perforin lysed tumor target cells about 10-fold more efficiently than comparable effector cells without granzymes. Enucleated cytoplast targets derived from these cells were also lysed with a similar 10-fold effect of granzymes. In contrast to cytoplasts, effector granzyme expression did not influence lysis of red cell targets. The Fas pathway was assessed using the selected cytotoxic T lymphocyte hybridoma subline d11S, which lysed target cells expressing Fas but not those lacking Fas. Similarly, cytoplasts derived from Fas+ but not Fas- cells were also readily lysed by these effector cells. Thus, neither the nucleus itself nor the characteristic apoptotic nuclear damage associated with the two major cell death pathways used by cytotoxic lymphocytes are required for cell death per se.

APA, Harvard, Vancouver, ISO, and other styles

42

Tang, Peter S., Marco Mura, Rashmi Seth, and Mingyao Liu. "Acute lung injury and cell death: how many ways can cells die?" American Journal of Physiology-Lung Cellular and Molecular Physiology 294, no. 4 (April 2008): L632—L641. http://dx.doi.org/10.1152/ajplung.00262.2007.

Full text

Abstract:

Apoptosis has been considered as an underlying mechanism in acute lung injury/acute respiratory distress syndrome and multiorgan dysfunction syndrome. Recently, several alternative pathways for cell death (such as caspase-independent cell death, oncosis, and autophagy) have been discovered. Evidence of these pathways in the pathogenesis of acute lung injury has also come into light. In this article, we briefly introduce cell death pathways and then focus on studies related to lung injury. The different types of cell death that occur and the underlying mechanisms utilized depend on both experimental and clinical conditions. Lipopolysaccharide-induced acute lung injury is associated with apoptosis via Fas/Fas ligand mechanisms. Hyperoxia and ischemia-reperfusion injury generate reactive oxidative species, which induce complex cell death patterns composed of apoptosis, oncosis, and necrosis. Prolonged overexpression of inflammatory mediators results in increased production and activation of proteases, especially cathepsins. Activation and resistance to death of neutrophils also plays an important role in promoting parenchymal cell death. Knowledge of the coexisting multiple cell death pathways and awareness of the pharmacological inhibitors targeting different proteases critical to cell death may lead to the development of novel therapies for acute lung injury.

APA, Harvard, Vancouver, ISO, and other styles

43

Dragovich, Tomislav, Charles M. Rudin, and Craig B. Thompson. "Signal transduction pathways that regulate cell survival and cell death." Oncogene 17, no. 25 (December 1998): 3207–13. http://dx.doi.org/10.1038/sj.onc.1202587.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Graham, Steven H., and Jun Chen. "Programmed Cell Death in Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 21, no. 2 (February 2001): 99–109. http://dx.doi.org/10.1097/00004647-200102000-00001.

Full text

Abstract:

Programmed cell death (PCD) is an ordered and tightly controlled set of changes in gene expression and protein activity that results in neuronal cell death during brain development. This article reviews the molecular pathways by which PCD is executed in mammalian cells and the potential relation of these pathways to pathologic neuronal cell death. Whereas the classical patterns of apoptotic morphologic change often do not appear in the brain after ischemia, there is emerging biochemical and pharmacologic evidence suggesting a role for PCD in ischemic brain injury. The most convincing evidence for the induction of PCD after ischemia includes the altered expression and activity in the ischemic brain of deduced key death-regulatory genes. Furthermore, studies have shown that alterations in the activity of these gene products by peptide inhibitors, viral vector-mediated gene transfer, antisense oligonucleotides, or transgenic mouse techniques determine, at least in part, whether ischemic neurons live or die after stroke. These studies provide strong support for the hypothesis that PCD contributes to neuronal cell death caused by ischemic injury. However, many questions remain regarding the precise pathways that initiate, sense, and transmit cell death signals in ischemic neurons and the molecular mechanisms by which neuronal cell death is executed at different stages of ischemic injury. Elucidation of these pathways and mechanisms may lead to the development of novel therapeutic strategies for brain injury after stroke and related neurologic disorders.

APA, Harvard, Vancouver, ISO, and other styles

45

Williams, Thomas J., Luis E. Gonzales-Huerta, and Darius Armstrong-James. "Fungal-Induced Programmed Cell Death." Journal of Fungi 7, no. 3 (March 20, 2021): 231. http://dx.doi.org/10.3390/jof7030231.

Full text

Abstract:

Fungal infections are a cause of morbidity in humans, and despite the availability of a range of antifungal treatments, the mortality rate remains unacceptably high. Although our knowledge of the interactions between pathogenic fungi and the host continues to grow, further research is still required to fully understand the mechanism underpinning fungal pathogenicity, which may provide new insights for the treatment of fungal disease. There is great interest regarding how microbes induce programmed cell death and what this means in terms of the immune response and resolution of infection as well as microbe-specific mechanisms that influence cell death pathways to aid in their survival and continued infection. Here, we discuss how programmed cell death is induced by fungi that commonly cause opportunistic infections, including Candida albicans, Aspergillus fumigatus, and Cryptococcus neoformans, the role of programmed cell death in fungal immunity, and how fungi manipulate these pathways.

APA, Harvard, Vancouver, ISO, and other styles

46

Hartman, Mariusz L. "Non-Apoptotic Cell Death Signaling Pathways in Melanoma." International Journal of Molecular Sciences 21, no. 8 (April 23, 2020): 2980. http://dx.doi.org/10.3390/ijms21082980.

Full text

Abstract:

Resisting cell death is a hallmark of cancer. Disturbances in the execution of cell death programs promote carcinogenesis and survival of cancer cells under unfavorable conditions, including exposition to anti-cancer therapies. Specific modalities of regulated cell death (RCD) have been classified based on different criteria, including morphological features, biochemical alterations and immunological consequences. Although melanoma cells are broadly equipped with the anti-apoptotic machinery and recurrent genetic alterations in the components of the RAS/RAF/MEK/ERK signaling markedly contribute to the pro-survival phenotype of melanoma, the roles of autophagy-dependent cell death, necroptosis, ferroptosis, pyroptosis, and parthanatos have recently gained great interest. These signaling cascades are involved in melanoma cell response and resistance to the therapeutics used in the clinic, including inhibitors of BRAFmut and MEK1/2, and immunotherapy. In addition, the relationships between sensitivity to non-apoptotic cell death routes and specific cell phenotypes have been demonstrated, suggesting that plasticity of melanoma cells can be exploited to modulate response of these cells to different cell death stimuli. In this review, the current knowledge on the non-apoptotic cell death signaling pathways in melanoma cell biology and response to anti-cancer drugs has been discussed.

APA, Harvard, Vancouver, ISO, and other styles

47

Basmaciyan, Louise, and Magali Casanova. "Cell death in Leishmania." Parasite 26 (2019): 71. http://dx.doi.org/10.1051/parasite/2019071.

Full text

Abstract:

Leishmaniases still represent a global scourge and new therapeutic tools are necessary to replace the current expensive, difficult to administer treatments that induce numerous adverse effects and for which resistance is increasingly worrying. In this context, the particularly original organization of the Leishmania parasite in comparison to higher eukaryotes is a great advantage. It allows for the development of new, very specific, and thus non-cytotoxic treatments. Among these originalities, Leishmania cell death can be cited. Despite a classic pattern of apoptosis, key mammalian apoptotic proteins are not present in Leishmania, such as caspases, cell death receptors, and anti-apoptotic molecules. Recent studies have helped to develop a better understanding of parasite cell death, identifying new proteins or even new apoptotic pathways. This review provides an overview of the current knowledge on Leishmania cell death, describing its physiological roles and its phenotype, and discusses the involvement of various proteins: endonuclease G, metacaspase, aquaporin Li-BH3AQP, calpains, cysteine proteinase C, LmjHYD36 and Lmj.22.0600. From these data, potential apoptotic pathways are suggested. This review also offers tools to identify new Leishmania cell death effectors. Lastly, different approaches to use this knowledge for the development of new therapeutic tools are suggested: either inhibition of Leishmania cell death or activation of cell death for instance by treating cells with proteins or peptides involved in parasite death fused to a cell permeant peptide or encapsulated into a lipidic vector to target intra-macrophagic Leishmania cells.

APA, Harvard, Vancouver, ISO, and other styles

48

Michel, Patrick P., Etienne C. Hirsch, and Stéphane Hunot. "Understanding Dopaminergic Cell Death Pathways in Parkinson Disease." Neuron 90, no. 4 (May 2016): 675–91. http://dx.doi.org/10.1016/j.neuron.2016.03.038.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Mroz, Pawel, Anastasia Yaroslavsky, Gitika B. Kharkwal, and Michael R. Hamblin. "Cell Death Pathways in Photodynamic Therapy of Cancer." Cancers 3, no. 2 (June 3, 2011): 2516–39. http://dx.doi.org/10.3390/cancers3022516.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Neitemeier, Sandra, Anja Jelinek, Vincenzo Laino, Lena Hoffmann, Ina Eisenbach, Roman Eying, Goutham K. Ganjam, Amalia M. Dolga, Sina Oppermann, and Carsten Culmsee. "BID links ferroptosis to mitochondrial cell death pathways." Redox Biology 12 (August 2017): 558–70. http://dx.doi.org/10.1016/j.redox.2017.03.007.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!