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Crosstalk between apoptosis.; necrosis and autophagy
Open accessAbstract
Apoptosis and necrosis are the two major modes of cell death, the molecular mechanisms of which have been extensively studied. Although initially thought to constitute mutually exclusive cellular states, recent findings reveal cellular contexts that require a balanced interplay between these two modes of cellular demise. Several death initiator and effector molecules, signaling pathways and subcellular sites have been identified as key mediators in both processes, either by constituting common modules or alternatively by functioning as a switch allowing cells to decide which route to take, depending on the specific situation. Importantly, autophagy, which is a predominantly cytoprotective process, has been linked to both types of cell death, serving either a pro-survival or pro-death function. Here we review the recent literature that highlights the intricate interplay between apoptosis, necrosis and autophagy, focusing on the relevance and impact of this crosstalk in normal development and in pathology. This article is part of a Special Section entitled: Cell Death Pathways.
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“While autophagy is implicated in several paradigms of life extension and is generally considered an antiaging mechanism, autophagy is also a well-defined mechanism of cell death, autophagy-dependent cell death, ADCD [153,154,155].”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [153]
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Chang, B.-P., Wang, D., Xing, J., Yang, S., Chu, Q., & Yu, S. (2014) · Journal of Huazhong University of Science and Technology [Medical Sciences] · doi:10.1007/s11596-014-1259-3 · Cited by 41
Yu, C., Kim, B., & Kim, E. (2016) · Cell Death and Differentiation · doi:10.1038/cdd.2016.99 · Cited by 42
“Such a dual role in promoting different types of cell death has been shown for p53, which can trigger both apoptosis and necrosis in response to multiple cellular insults.(47) However, the subcellular localization of p53 does not appear to determine the type of cell death that it promotes.”
BackgroundEpac: new emerging cAMP-binding protein
Lee, K. (2021) · BMB Reports · doi:10.5483/bmbrep.2021.54.3.233 · Cited by 41
Urtasun, R., Elizalde, M., Azkona, M., Latasa, M. U., García‐Irigoyen, O., Uriarte, I., Fernández‐Barrena, M. G., Vicent, S., Alonso, M. M., Muntané, J., et al. (2016) · Oncogene · doi:10.1038/onc.2015.517 · Cited by 40
Targeted Imaging for Cell Death in Cardiovascular Disorders
Shekhar, A. C., Heeger, P. S., Reutelingsperger, C. P. M., Arbustini, E., Narula, N., Hofstra, L., Bax, J. J., & Narula, J. (2018) · JACC. Cardiovascular imaging · doi:10.1016/j.jcmg.2017.11.018 · Cited by 39
“It appears that many of these pathways share elements and can influence each other (8,9).”
BackgroundG9a Promotes Breast Cancer Recurrence through Repression of a Pro-inflammatory Program
Mabe, N. W., Garcia, N. M. G., Wolery, S. E., Newcomb, R., Meingasner, R. C., Vilona, B. A., Lupo, R., Lin, C., Chi, J., & Alvarez, J. V. (2020) · Cell Reports · doi:10.1016/j.celrep.2020.108341 · Cited by 40
“Because TNF can induce both apoptotic and necroptotic cell death pathways (Laster et al., 1988; Nikoletopoulou et al., 2013), we next sought to define the mode of cell death following G9a inhibition.”
Exploring the Role of Autophagy Dysfunction in Neurodegenerative Disorders
Rana, T., Behl, T., Sehgal, A., Mehta, V., Singh, S., Bhatia, S., Al‐Harrasi, A., & BUNGAU, S. G. (2021) · Molecular Neurobiology · doi:10.1007/s12035-021-02472-0 · Cited by 42
Targeted Therapy of Spinal Cord Injury: Inhibition of Apoptosis Is a Promising Therapeutic Strategy
He, W., Li, Z., Gu, H.-Y., Pan, Q.-L., & Lin, F.-X. (2023) · Molecular Neurobiology · doi:10.1007/s12035-023-03814-w · Cited by 39
“Necroptosis is initiated by many members of the death receptor and pathogen recognition receptor family, including TNFR1, FAS, and TNFR2 [42] (Fig.”
Autophagy postpones apoptotic cell death in PRRSV infection through Bad-Beclin1 interaction
Zhou, A., Li, S., Khan, F. A., & Zhang, S. (2015) · Virulence · doi:10.1080/21505594.2015.1131381 · Cited by 39
Alnasser, H. A., Guan, Q., Zhang, F., Gleave, M. E., Nguan, C. Y. C., & Du, C. (2015) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00304.2015 · Cited by 37
Vitamin C induces apoptosis in AGS cells via production of ROS of mitochondria
Lim, J. Y., Kim, D.-H., Kim, B. R., Jun, J., Yeom, J. S., Park, J. S., Seo, J., Park, C. H., Woo, H. O., Youn, H., et al. (2016) · Oncology Letters · doi:10.3892/ol.2016.5212 · Cited by 39
Autophagy and the invisible line between life and death
Swart, C., du Toit, A., & Loos, B. (2016) · European Journal of Cell Biology · doi:10.1016/j.ejcb.2016.10.005 · Cited by 40
Regulation of BECN1-mediated autophagy by HSPB6: Insights from a human HSPB6 S10F mutant
Liu, G., Zhu, H., Cai, W., Wang, X., Jiang, M., Essandoh, K., Vafiadaki, E., Haghighi, K., Lam, C. K., Gardner, G., et al. (2017) · Autophagy · doi:10.1080/15548627.2017.1392420 · Cited by 40
“The primary function of autophagy is to maintain cellular homeostasis and promote cell survival.(20) Inhibition of autophagy causes accumulation of cytoplasmic components and induction of apoptosis.”
BackgroundHyperglycemia potentiates a shift from apoptosis to RIP1-dependent necroptosis
McCaig, W. D., Patel, P., Sosunov, S. A., Shakerley, N. L., Smiraglia, T., Craft, M. M., Walker, K. M., Deragon, M. A., Ten, V. S., & LaRocca, T. J. (2018) · Cell Death Discovery · doi:10.1038/s41420-018-0058-1 · Cited by 39
YU, W.-N., LAI, Y.-J., Ma, J.-W., Ho, C., HUNG, S.-W., Chen, Y.-H., Chen, C.-T., Kao, J., & Way, T. (2019) · In Vivo · doi:10.21873/invivo.11590 · Cited by 40
Brokaw, D. L., Piras, I. S., Mastroeni, D., Weisenberger, D. J., Nolz, J., Delvaux, E., Serrano, G. E., Beach, T. G., Huentelman, M. J., & Coleman, P. D. (2020) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2020.06.022 · Cited by 38
“, 2015), the MAPK (Kim and Choi, 2015; Wagner and Nebreda, 2009), and NFκB (Bours et al., 2000; Lawrence, 2009; Nikoletopoulou et al., 2013; Pires et al., 2018) signaling pathways.”
Cervical cancer: a meta-analysis, therapy and future of nanomedicine
Venkatas, J., & Singh, M. (2020) · ecancermedicalscience · doi:10.3332/ecancer.2020.1111 · Cited by 39
Brodarac, A., Šarić, T., Oberwallner, B., Mahmoodzadeh, S., Neef, K., Albrecht, J., Burkert, K., Oliverio, M., Nguemo, F., Choi, Y., et al. (2015) · Stem Cell Research & Therapy · doi:10.1186/s13287-015-0057-6 · Cited by 39
“These findings mirror a substantial cell damage and are in line with studies showing that dying cells display characteristics of apoptosis, autophagy and necrosis at the same time [26].”
ResultZhou, S., Wang, Y., Yang, Y., He, Z., Zhao, R., Zhe, H., Zhang, X., Pan, S., Duan, W., Yang, T., et al. (2015) · Drug Design Development and Therapy · doi:10.2147/dddt.s73493 · Cited by 39
Chan, C. K., Chan, G., Awang, K., & Kadir, H. A. (2016) · Molecules · doi:10.3390/molecules21030385 · Cited by 40
“Cell death is the outcome of three well known dynamic cellular activities such as apoptosis, autophagy and necrosis [28].”
BackgroundFerroptosis in tumors and its relationship to other programmed cell death: role of non-coding RNAs
Zhang, Q., Fan, X., Zhang, X., & Ju, S. (2023) · Journal of Translational Medicine · doi:10.1186/s12967-023-04370-6 · Cited by 39
Autophagic flux and autophagosome morphogenesis require the participation of sphingolipids
Tommasino, C., Marconi, M., Ciarlo, L., Matarrese, P., & Malorni, W. (2015) · APOPTOSIS · doi:10.1007/s10495-015-1102-8 · Cited by 39
“On the other hand, p53 could stimulate autophagy by inhibiting mTOR via activation of the AMPK or through the transactivation of damage-regulated autophagy modulator (DRAM), a direct p53 target gene encoding a lysosomal protein that induces autophagy [27].”
InfluentialPhilipp, S., Sosna, J., Plenge, J., Kalthoff, H., & Adam, D. (2015) · Cell Communication and Signaling · doi:10.1186/s12964-015-0103-0 · Cited by 38
“In necroptosis triggered by death receptors, activation of RIPK1 and RIPK3 to form the necrosome is a critical event [44].”
BackgroundAging and uremia: Is there cellular and molecular crossover?
White, W. E. (2015) · World Journal of Nephrology · doi:10.5527/wjn.v4.i1.19 · Cited by 38
Insights into the in vitro Anticancer Effects of Diruthenium‐1
Koceva‐Chyła, A., Matczak, K., Hikisz, P., Durka, M. K., Kochel, K., Süß‐Fink, G., Furrer, J., & Kowalski, K. (2016) · ChemMedChem · doi:10.1002/cmdc.201600315 · Cited by 38
Ciechomska, I. A., Marciniak, M. P., Jackl, J., & Kaminska, B. (2018) · Frontiers in Pharmacology · doi:10.3389/fphar.2018.01271 · Cited by 41
Levada, K. V., Pshenichnikov, S. E., Omelyanchik, A. S., Rodionova, V. V., Nikitin, A. A., Савченко, А. Г., Щетинин, И. В., Zhukov, D., Abakumov, M. A., Majouga, A. G., et al. (2020) · Nano Convergence · doi:10.1186/s40580-020-00228-5 · Cited by 38
Serrano‐Heras, G., Cicuéndez, I. D.-M., Castro‐Robles, B., Carrión, B., Moratalla, A. B. P., Gil, J. G., Arteaga, S., Hernández‐Fernández, F., García‐García, J., Martín, Ó. A., et al. (2020) · Biological Procedures Online · doi:10.1186/s12575-020-00130-8 · Cited by 38
“Funding This research was supported by a grant (number: PI12/01544) from the Instituto de Salud Carlos III (Spanish Ministry of Economy and Competitiveness) and co-financed by European Regional Development Fund (FEDER).”
BackgroundInfluentialSun, X., Zhang, J., Guo, Y.-X., Xia, T., Xu, L., Rahmand, K., Wang, G.-P., Li, X.-J., Han, T., Wang, N., et al. (2021) · Journal of Pharmacy and Pharmacology · doi:10.1093/jpp/rgab052 · Cited by 39
Xin, P., Xu, L., Dong, W., Mao, L., Guo, J., Bi, J., Zhang, S., Pei, Y., & Chen, C. (2022) · Angewandte Chemie International Edition · doi:10.1002/anie.202217859 · Cited by 37
Juliano, R. L., Wang, L., Tavares, F. X., Brown, E., James, L. I., Ariyarathna, Y., Ming, X., Mao, C., & Suto, M. J. (2018) · Nucleic Acids Research · doi:10.1093/nar/gkx1320 · Cited by 37
Polloni, L., Seni-Silva, A. C., Teixeira, S. C., Azevedo, F. V. P. D. V., Zóia, M. A. P., da Silva, M. S., Lima, P. M. A. P., Correia, L. I. V., Almeida, J. D. C., da Silva, C. V., et al. (2019) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2019.01.047 · Cited by 39
Enhanced Autophagy Contributes to Reduced Viral Infection in Black Flying Fox Cells
Laing, E. D., Sterling, S. L., Weir, D. L., Beauregard, C. R., Smith, I., Larsen, S. E., Wang, L., Snow, A. L., Schaefer, B. C., & Broder, C. C. (2019) · Viruses · doi:10.3390/v11030260 · Cited by 38
“, nutrient deprivation) or itself act as a mechanism of programmed cell death if left unchecked [78,79].”
Background
Metadata
- Authors
- Nikoletopoulou, V., Markaki, M., Palikaras, K., & Tavernarakis, N.
- Affiliations
- Foundation for Research and Technology Hellas (GR)
- Corresponding author
- Tavernarakis, Nektarios
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
- Publisher
- Elsevier BV
- Published
- 2013-12
- Volume
- 1833
- Issue
- 12
- Pages
- 3448-3459
- ISSN
- 0167-4889 (ISSN-L)
- OpenAlex
- W2059738518
- Cited by
- 1,366
- References
- 150
- Citations by year
- 2026: 43 · 2025: 58 · 2024: 80 · 2023: 91 · 2022: 113 · 2021: 147 · 2020: 133 · 2019: 146 · 2018: 136 · 2017: 141 · 2016: 122 · 2015: 107 · 2014: 43 · 2013: 5
- FWCI
- 8.50
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research (publishedVersion)
- PubMed (publishedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Funders
- European Research Council
- Ministry of National Education and Religious Affairs
- European Molecular Biology Organization
- Seventh Framework Programme
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Social Sciences › Anthropology › Death, Funerary Practices, and Mourning
- Keywords
- apoptosis, necrosis, autophagy, cell death crosstalk, cell death pathways, cell fate determination, development (biology), disease pathology
- MeSH terms
- Autophagy, Humans, Models, Biological, Necrosis, Signal Transduction, Apoptosis
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