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The Cell Non-Autonomous Nature of Electron Transport Chain-Mediated Longevity
Open accessAbstract
The life span of C. elegans can be increased via reduced function of the mitochondria; however, the extent to which mitochondrial alteration in a single, distinct tissue may influence aging in the whole organism remains unknown. We addressed this question by asking whether manipulations to ETC function can modulate aging in a cell-non-autonomous fashion. We report that the alteration of mitochondrial function in key tissues is essential for establishing and maintaining a prolongevity cue. We find that regulators of mitochondrial stress responses are essential and specific genetic requirements for the electron transport chain (ETC) longevity pathway. Strikingly, we find that mitochondrial perturbation in one tissue is perceived and acted upon by the mitochondrial stress response pathway in a distal tissue. These results suggest that mitochondria may establish and perpetuate the rate of aging for the whole organism independent of cell-autonomous functions.
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“Such hormetic reactions may consist in the induction of a mitochondrial stress response either in the same tissue in which mitochondria are defective, or even in distant tissues, as shown in C. elegans”
From The Hallmarks of Aging (2013) · cites this paper as Durieux et al., 2011
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“Conversely, lifespan-extending manipulations targeting one single tissue can retard the aging process in other tissues (Durieux et al., 2011; Lavasani et al., 2012; Tomas-Loba et al., 2008).”
From The Hallmarks of Aging (2013) · cites this paper as Durieux et al., 2011
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“Interestingly, mild mitochondrial stress might elicit beneficial effects on health and lifespan through the activation of mitochondrial hormesis [28,36].”
From Inhibition of the Fission Machinery Mitigates OPA1 Impairment in Adult Skeletal Muscles (2019) · cites this paper as [36]
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Biochemical Genetic Pathways that Modulate Aging in Multiple Species: Figure 1.Preprint
Bitto, A., Wang, A. M., Bennett, C. F., & Kaeberlein, M. R. (2015) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a025114 · Cited by 122
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Burtscher, J., Soltany, A., Visavadiya, N. P., Burtscher, M., Millet, G. P., Khoramipour, K., & Khamoui, A. V. (2023) · Aging Cell · doi:10.1111/acel.13770 · Cited by 123
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InfluentialTwo conserved epigenetic regulators prevent healthy ageing
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BackgroundInfluentialCytosolic Proteostasis Networks of the Mitochondrial Stress Response
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BackgroundInfluentialComplex IV-deficient Surf1−/− mice initiate mitochondrial stress responses
Pulliam, D. A., Deepa, S. S., Liu, Y., Hill, S., Lin, A., Bhattacharya, A., Shi, Y., Sloane, L. B., Viscomi, C. F., Zeviani, M., et al. (2014) · Biochemical Journal · doi:10.1042/bj20140291 · Cited by 111
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BackgroundMitophagy plays a central role in mitochondrial ageing
Diot, A., Morten, K., & Poulton, J. (2016) · Mammalian Genome · doi:10.1007/s00335-016-9651-x · Cited by 112
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Structural and Functional Rescue of Chronic Metabolically Stressed Optic Nerves through Respiration
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“Mitochondrial perturbation in one cell or tissue can dictate mitochondrial stress response in another (Durieux et al., 2011).”
BackgroundMitochondrial Stress Signaling Promotes Cellular Adaptations
Barbour, J. A., & Turner, N. A. (2014) · International Journal of Cell Biology · doi:10.1155/2014/156020 · Cited by 108
“elegans induces mtUPR induction in the gut, which provides evidence for cellular adaptations to mitochondrial stress in a noncell autonomous manner [130].”
BackgroundThe paradox of mitochondrial dysfunction and extended longevity
Munkácsy, E., & Rea, S. L. (2014) · Experimental Gerontology · doi:10.1016/j.exger.2014.03.016 · Cited by 103
The social nature of mitochondria: Implications for human health
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Cell non-autonomous regulation of health and longevity
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“In addition, lifespan studies of C. elegans with genetic manipulation increasing stress resistance suggest that the stress response pathway is an important mechanism for regulating lifespan (Durieux et al., 2011; Taylor and Dillin, 2013).”
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“This seems unlikely in the case of the UPR as the beneficial effects of this pathway have also been proposed to be most relevant early in life [54].”
BackgroundThe complex crosstalk between mitochondria and the nucleus: What goes in between?
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BackgroundPrinciples of the Molecular and Cellular Mechanisms of Aging
da Silva, P. F. L., & Schumacher, B. (2021) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2020.11.018 · Cited by 106
The mitochondrial unfolded protein response and mitohormesis: a perspective on metabolic diseases
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Visible light reduces C. elegans longevity
Filho, C. D. D. M., Henriquez, B., Seah, N., Evans, R. M., Lapierre, L. R., & Dillin, A. G. (2018) · Nature Communications · doi:10.1038/s41467-018-02934-5 · Cited by 100
Cell-Nonautonomous Regulation of Proteostasis in Aging and DiseasePreprint
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“The observations on cell-nonautonomous control of the HSR extend to the UPR and the UPR (Durieux et al. 2011; Imanikia et al. 2018; Martínez et al. 2018; Zhang et al. 2018).”
BackgroundInfluentialPINK1/Parkin-Dependent Mitochondrial Surveillance: From Pleiotropy to Parkinson's Disease
Mouton‐Liger, F., Jacoupy, M., Corvol, J., & Corti, O. (2017) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2017.00120 · Cited by 100
“Moreover, several studies linked UPRmt activation associated with mitochondrial dysfunction with organismal lifespan extension, although whether UPRmt is indispensable for increased longevity is debated (Durieux et al., 2011; Houtkooper et al., 2013; Schieber and Chandel, 2014; Schulz and Haynes, 2015).”
Integrated stress response stimulates FGF21 expression: Systemic enhancer of longevity
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“[89] demonstrated in Caenorhabditis elegans that the mitochondrial stress-induced mtUPR in the nervous system generated a similar mtUPR in intestine, indicating that the stimulation of mtUPR could be transferred between tissues.”
BackgroundAge-Related Oxidative Stress Compromises Endosomal Proteostasis
Cannizzo, E. S., Clement, C. C., Morozova, K., Valdor, R., Kaushik, S., Almeida, L. N., Follo, C., Sahu, R., Cuervo, A. M., Macian, F., et al. (2012) · Cell Reports · doi:10.1016/j.celrep.2012.06.005 · Cited by 95
“…oxidation of proteins, carbohydrates, lipids, and nucleic acids, a process generally known as oxidative stress (Broadley and Hartl, 2008; Alexeyev, 2009; Halliwell, 2009; Roberts and Sindhu, 2009; Hamanaka and Chandel, 2010; Wellen and Thompson, 2010; Cannizzo et al., 2011; Durieux et al., 2011).”
How the Mitoprotein-Induced Stress Response Safeguards the Cytosol: A Unified View
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“…in C. elegans, subsequent work has identified ATFS-1 and DVE-1/ UBL5 as important transcriptional activators of the UPR mt (Benedetti et al., 2006; Durieux et al., 2011; Fiorese et al., 2016; Gitschlag et al., 2016; Haynes et al., 2007, 2010; Lin et al., 2016; Lisanti et al., 2016; Merkwirth et…”
Sulforaphane promotes C. elegans longevity and healthspan via DAF-16/DAF-2 insulin/IGF-1 signaling
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Mitohormesis in Hypothalamic POMC Neurons Mediates Regular Exercise-Induced High-Turnover Metabolism
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“elegans, mitochondrial perturbation, introduced early in life during development and young adulthood, induced beneficial effects (Cox et al., 2018; Durieux et al., 2011; Schulz et al., 2007).”
InfluentialZhou, Z., Fan, Y., Zong, R., & Tan, K. (2022) · Ageing Research Reviews · doi:10.1016/j.arr.2022.101702 · Cited by 100
Inhibition of the Fission Machinery Mitigates OPA1 Impairment in Adult Skeletal Muscles
Romanello, V., Scalabrin, M., Albiero, M., Blaauw, B., Scorrano, L., & Sandri, M. (2019) · Cells · doi:10.3390/cells8060597 · Cited by 91
“Interestingly, mild mitochondrial stress might elicit beneficial effects on health and lifespan through the activation of mitochondrial hormesis [28,36].”
BackgroundZhang, Y., Zhang, W.-H., Zhang, P., Li, Q., Sun, Y., Wang, J., Zhang, S. O., Cai, T., Zhan, C., & Dong, M. (2022) · Nature Communications · doi:10.1038/s41467-022-33850-4 · Cited by 99
Age-Related Phasic Patterns of Mitochondrial Maintenance in Adult Caenorhabditis elegans Neurons
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“Alternatively, as neurons have been shown to regulate animal life span (Bishop and Guarente, 2007; Wolkow et al., 2000; Durieux et al., 2011), age-related decline of neuronal mitochondrial load may exacerbate physiological aging of the animal by affecting neuronal signaling.”
BackgroundSelected mitochondrial DNA landscapes activate the SIRT3 axis of the UPRmt to promote metastasis
Kenny, T. C., Hart, P. C., Ragazzi, M., Sersinghe, M., Chipuk, J. E., Sagar, M. A. K., Eliceiri, K. W., LaFramboise, T., Grandhi, S., Santos, J. H., et al. (2017) · Oncogene · doi:10.1038/onc.2017.52 · Cited by 93
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“UPR can be triggered by excessive protein misfolding (67), inhibition of mitochondrial transcription and translation (69), impaired electron transport chain activity, and increased ROS levels (70).”
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Organismal proteostasis: role of cell-nonautonomous regulation and transcellular chaperone signalingPreprint
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“1B) and, in this sense, compensates for the repression of HSF-1.”
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The role of hydrogen sulfide in aging and age-related pathologies
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“The age-associated alterations in intercellular communication also explain the interorgan coordination of aging, in which lifespan-extending manipulations in one tissue were described to retard the aging process in other tissues [279-282].”
BackgroundProtein trafficking at the crossroads to mitochondria
Wasilewski, M., Chojnacka, K., & Chacińska, A. (2016) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2016.10.019 · Cited by 95
“Proteotoxic stress that is elicited in a single tissue in awormcan induce theUPRmt in another tissue and extend the lifespan of the organism as awhole [214].”
Background“Photobiomics”: Can Light, Including Photobiomodulation, Alter the Microbiome?
Liebert, A. D., Bicknell, B. T., Johnstone, D. M., Gordon, L. C., Kiat, H., & Hamblin, M. R. (2019) · Photobiomodulation Photomedicine and Laser Surgery · doi:10.1089/photob.2019.4628 · Cited by 88
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Proteotoxic stress and ageing triggers the loss of redox homeostasis across cellular compartments
Kirstein, J., Morito, D., Kakihana, T., Sugihara, M., Minnen, A., Hipp, M. S., Nussbaum-Krammer, C. I., Kasturi, P., Hartl, F. U., Nagata, K., et al. (2015) · The EMBO Journal · doi:10.15252/embj.201591711 · Cited by 90
“…has been established that stress response pathways can also be regulated in a cell non-autonomous manner and that tissues can orchestrate an organismal-wide stress response (Prahlad et al , 2008; Durieux et al , 2011; Prahlad & Morimoto, 2011; van Oosten-Hawle et al , 2013; Taylor & Dillin, 2013).”
Chlorogenic Acid Extends the Lifespan ofCaenorhabditis elegansvia Insulin/IGF-1 Signaling Pathway
Zheng, S., Huang, X., Xing, T.-K., Ding, A.-J., Wu, G.-S., & Luo, H. (2016) · The Journals of Gerontology Series A · doi:10.1093/gerona/glw105 · Cited by 89
Lysosome lipid signalling from the periphery to neurons regulates longevity
Savini, M., Folick, A., Lee, Y.-T., Jin, F., Cuevas, A. R., Tillman, M. C., Duffy, J., Zhao, Q., Neve, I. A. A., Hu, P.-W., et al. (2022) · Nature Cell Biology · doi:10.1038/s41556-022-00926-8 · Cited by 89
Mitochondria and Organismal Longevity
Hwang, A. B., Jeong, D., & Lee, S. (2012) · Current Genomics · doi:10.2174/138920212803251427 · Cited by 87
Linton, P., & Thoman, M. L. (2014) · Immunology Letters · doi:10.1016/j.imlet.2014.06.017 · Cited by 87
“In aging cells an imbalance due to increased ROS production and a decrease in the levels of activity of the ROS-converting enzymes, leads to the nonenzymatic oxidation of proteins, carbohydrates, lipids and nucleic acids, a process generally known as oxidative stress[99-105].”
BackgroundSystemic effects of mitochondrial stress
Bar‐Ziv, R., Bolas, T., & Dillin, A. G. (2020) · EMBO Reports · doi:10.15252/embr.202050094 · Cited by 86
“In a study from our group in 2011 [100], the effects of triggering mitochondrial stress in specific tissues was directly tested in C. elegans .”
Han, S. M., Tsuda, H., Yang, Y., Vibbert, J., Cottee, P. A., Lee, S.-J., Winek, J., Haueter, C. M., Bellen, H. J., & Miller, M. A. (2012) · Developmental Cell · doi:10.1016/j.devcel.2011.12.009 · Cited by 87
“depleted SAX-3 in body wall muscle of wild-type worms using an RNAi mosaic strategy (Durieux et al., 2011; Esposito et al., 2007).”
Neuronal Responses to Physiological Stress
Kagias, K., Nehammer, C., & Pocock, R. (2012) · Frontiers in Genetics · doi:10.3389/fgene.2012.00222 · Cited by 94
“elegans induces the mitochondria-specific unfolded protein response in intestinal cells, thus increasing the lifespan of the animals (Durieux et al., 2011).”
BackgroundKlotho: An Elephant in Aging Research
Cheikhi, A., Barchowsky, A., Sahu, A., Shinde, S. N., Pius, A., Clemens, Z. J., Li, H., Kennedy, C. A., Hoeck, J. D., Franti, M., et al. (2019) · The Journals of Gerontology: Series A · doi:10.1093/gerona/glz061 · Cited by 92
Physiological consequences of complex II inhibition for aging, disease, and the mKATP channel
Wojtovich, A. P., Smith, C. O., Haynes, C. M., Nehrke, K. W., & Brookes, P. S. (2013) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/j.bbabio.2012.12.007 · Cited by 86
“pear to respond to mitochondrial dysfunction as well [78,81–84].”
BackgroundHekimi, S., Wang, Y., & Noë, A. (2016) · Frontiers in Genetics · doi:10.3389/fgene.2016.00161 · Cited by 83
“Finally, in this regard, it has been proposed that induction of mitochondrial unfolded protein response (UPRmt) promotes longevity and is directly responsible for the lifespan extension from ETC inhibition (Yang and Hekimi, 2010b; Durieux et al., 2011).”
BackgroundMetabolic Communication and Healthy Aging: Where Should We Focus Our Energy?
Smith, H. J., Sharma, A., & Mair, W. B. (2020) · Developmental Cell · doi:10.1016/j.devcel.2020.06.011 · Cited by 83
The Mitochondria-Regulated Immune Pathway Activated in the C. elegans Intestine Is Neuroprotective
Chikka, M. R., Anbalagan, C., Dvorak, K., Dombeck, K., & Prahlad, V. (2016) · Cell Reports · doi:10.1016/j.celrep.2016.07.077 · Cited by 83
“elegans, activation of UPR in neuronal cells affects UPR in the intestine (Durieux et al., 2011), we examined whether UPR-mediated signaling could allow for the observed cell-non-autonomous neuronal protection.”
Ewald, C. Y., Hourihan, J. M., Bland, M. S., Obieglo, C., Katic, I., Mazzeo, L. E. M., Alcedo, J., Blackwell, T. K., & Hynes, N. E. (2017) · eLife · doi:10.7554/elife.19493 · Cited by 88
“…(ROS) affect aging is a fundamental issue in biology (Back et al., 2012a; Krause, 2007; Hekimi et al., 2011; Ristow, 2014; Ristow and Schmeisser, 2014; Kawagishi and Finkel, 2014; Riera and Dillin, 2015; Durieux et al., 2011; Balaban et al., 2005; Melov, 2002; Shadel, 2014; Sena and Chandel, 2012).”
BackgroundTaylor, R. C. (2016) · Brain Research · doi:10.1016/j.brainres.2016.04.017 · Cited by 83
“…stress responses, signaling pathways that detect misfolded proteins and other perturbations to cellular homeostasis in specific organelles, and that activate defensive responses to alleviate or adapt cells to stress (Durieux et al., 2011; Morley and Morimoto, 2004; Taylor and Dillin, 2013).”
BackgroundOxidative stress and exceptional human longevity: Systematic review
Belenguer‐Varea, Á., Tarazona‐Santabalbina, F. J., Avellana-Zaragoza, J. A., Martínez-Reig, M., Mas‐Bargues, C., & Inglés, M. (2019) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2019.09.019 · Cited by 86
Ploumi, C., Kyriakakis, E., & Tavernarakis, N. (2023) · Cell Death and Disease · doi:10.1038/s41419-023-05638-x · Cited by 85
“Perturbation of ETC function activates the mitochondrial unfolded protein response (UPR), a stress defense mechanism, required for ETC perturbation-mediated longevity [30, 31].”
BackgroundLiang, V., Ullrich, M., Lam, H., Chew, Y. L., Banister, S. D., Song, X., Zaw, T., Kassiou, M., Götz, J., & Nicholas, H. (2014) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-014-1558-7 · Cited by 85
Mitochondrial Function and Dysfunction: An Update
Davis, R. E., & Williams, M. J. (2012) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.112.192104 · Cited by 91
“…theory of aging that reflects the negative impact of chronic, accumulating damage to DNA and cellular proteins from free radicals as a function of age (Kujoth et al., 2005; Wallace, 2005; Dagda et al., 2009; Swerdlow and Kahn, 2009; Lapointe and Hekimi, 2010; Durieux et al., 2011; Pamplona, 2011).”
BackgroundMitochondrial Quality Control Mechanisms and the PHB (Prohibitin) Complex
Hernando‐Rodríguez, B., & Artal‐Sanz, M. (2018) · Cells · doi:10.3390/cells7120238 · Cited by 90
“Interestingly, depletion of mitochondrial components only during development is sufficient to enhance lifespan, whereas reduction of gene expression during adulthood, even though it decreases ATP production, it does not affect lifespan [48,61,75,76].”
BackgroundZhang, B., Gong, J., Zhang, W., Xiao, R., Liu, J., & Xu, X. Z. S. (2018) · Genes & Development · doi:10.1101/gad.309625.117 · Cited by 88
“Calcium imaging experiments were conducted on an Olympus upright microscope (BX51WI) under a 60× objective as described previously (Feng et al. 2006; Li et al. 2006).”
Mitochondrial uncoupling and longevity – A role for mitokines?
Klaus, S., & Ost, M. (2019) · Experimental Gerontology · doi:10.1016/j.exger.2019.110796 · Cited by 80
Conte, M., Sabbatinelli, J., Chiariello, A., Martucci, M., Santoro, A., Monti, D., Arcaro, M., Galimberti, D., Scarpini, E. A., Bonfigli, A. R., et al. (2020) · GeroScience · doi:10.1007/s11357-020-00287-w · Cited by 87
Denzel, M. S., Lapierre, L. R., & Mack, H. I. D. (2018) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2018.08.001 · Cited by 82
IGF‐I regulates the age‐dependent signaling peptide humanin
Lee, C., Wan, J., Miyazaki, B., Fang, Y., Guevara‐Aguirre, J., Yen, K., Longo, V., Bartke, A., & Cohen, P. (2014) · Aging Cell · doi:10.1111/acel.12243 · Cited by 80
“elegans, a stress-induced tissue-specific signal originating from mitochondria has been shown to communicate with distant organs and extend lifespan; the exact identity of this signal, termed ‘mitokine’, is unknown and currently being investigated (Durieux et al., 2011).”
BackgroundLi, T. Y., Sleiman, M. B., Li, H., Gao, A. W., Mottis, A., Bachmann, A. M., Alam, G. E., Li, X., Goeminne, L. J. E., Schoonjans, K., et al. (2021) · Nature Aging · doi:10.1038/s43587-020-00025-z · Cited by 78
Protein Quality Control in Health and DiseasePreprint
Dubnikov, T., Ben‐Gedalya, T., & Cohen, E. (2016) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a023523 · Cited by 82
“Similarly, UPR is activated in the nematode intestine by the inhibition of the electron transport chain in neurons (Durieux et al. 2011).”
BackgroundTOR Signaling Couples Oxygen Sensing to Lifespan in C. elegans
Schieber, M., & Chandel, N. S. (2014) · Cell Reports · doi:10.1016/j.celrep.2014.08.075 · Cited by 80
“The mitochondrial unfolded protein response (UPRmt) specifically activated in the intestine triggers a cell-non-autonomous signaling response to extend C. elegans lifespan (Durieux et al., 2011).”
BackgroundInfluentialIschemic preconditioning: The role of mitochondria and aging
Wojtovich, A. P., Nadtochiy, S. M., Brookes, P. S., & Nehrke, K. W. (2011) · Experimental Gerontology · doi:10.1016/j.exger.2011.11.001 · Cited by 79
“…(Yang and Hekimi, 2010) may coordinate functional responses; it is possible that these responses are not limited to the cell in which the signal originates, either, as recent data suggests that mitochondria can contribute to protection through trans-cellular signaling (Durieux et al., 2011).”
BackgroundTDP-1/TDP-43 Regulates Stress Signaling and Age-Dependent Proteotoxicity in Caenorhabditis elegans
Vaccaro, A., Tauffenberger, A., Ash, P. E. A., Carlomagno, Y., Petrucelli, L., & Parker, J. A. (2012) · PLoS Genetics · doi:10.1371/journal.pgen.1002806 · Cited by 79
“Cell non-autonomous signaling has been described in C. elegans for mitochondrial stress regulating longevity [43] and the heat shock response [44].”
Measuring Autophagy in Stressed Cells
Sharifi, M. N., Mowers, E. E., Drake, L. E., & Macleod, K. F. (2015) · Methods in molecular biology · doi:10.1007/978-1-4939-2522-3_10 · Cited by 80
“5Antibiotics, such as tetracycline and doxcycyline, inhibit mitochondrial protein translation, thereby inducing a “mitonuclear” protein imbalance and a mitochondrial unfolded protein response (UPRmt) [38, 39].”
BackgroundUPR ER promotes lipophagy independent of chaperones to extend life span
Daniele, J. R., Higuchi‐Sanabria, R., Durieux, J., Monshietehadi, S., Ramachandran, V., Tronnes, S. U., Kelet, N., Sanchez, M., Metcalf, M. G., Garcia, G., et al. (2020) · Science Advances · doi:10.1126/sciadv.aaz1441 · Cited by 79
Aging: All roads lead to mitochondria
Son, J. M., & Lee, C. D. (2021) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2021.02.006 · Cited by 86
Tian, J., Geiss, C., Zarse, K., Madreiter‐Sokolowski, C. T., & Ristow, M. (2021) · Aging · doi:10.18632/aging.203597 · Cited by 81
Unfolded protein stress in the endoplasmic reticulum and mitochondria: a role in neurodegeneration
Bernales, S., Morales-Soto, M. A., & McCullagh, E. (2012) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2012.00005 · Cited by 78
Walter, L., Baruah, A., Chang, H., Pace, H. M., & Lee, S. S. (2011) · PLoS Biology · doi:10.1371/journal.pbio.1001084 · Cited by 83
The Cellular Mitochondrial Genome Landscape in Disease
Hahn, A., & Zuryn, S. (2018) · Trends in Cell Biology · doi:10.1016/j.tcb.2018.11.004 · Cited by 75
Chatty Mitochondria: Keeping Balance in Cellular Protein Homeostasis
Topf, U., Wróbel, L., & Chacińska, A. (2016) · Trends in Cell Biology · doi:10.1016/j.tcb.2016.03.002 · Cited by 76
Mitochondria: multifaceted regulators of aging
Son, J. M., & Lee, C. D. (2019) · BMB Reports · doi:10.5483/bmbrep.2019.52.1.300 · Cited by 76
“, cco-1 knockdown) that exhibited extended lifespan (136).”
BackgroundTetracycline Antibiotics Induce Host-Dependent Disease Tolerance to Infection
Colaço, H. G., Barros, A., Neves‐Costa, A., Seixas, E., Pedroso, D. C. S., Velho, T. R., Willmann, K. L., Faísca, P., Grabmann, G., Yi, H., et al. (2020) · Immunity · doi:10.1016/j.immuni.2020.09.011 · Cited by 83
The yeast Tsa1 peroxiredoxin protects against protein aggregate-induced oxidative stress
Weids, A. J., & Grant, C. M. (2014) · Journal of Cell Science · doi:10.1242/jcs.144022 · Cited by 79
“Hsp104 is a stress-inducible protein disaggregase that has been used as an in situ marker for protein aggregation (Erjavec et al., 2007; Glover and Lindquist, 1998).”
Background
Metadata
- Authors
- Durieux, J., Wolff, S., & Dillin, A.
- Affiliations
- Salk Institute for Biological Studies (US)
- Scripps Research Institute (US)
- Corresponding author
- Dillin, Andrew
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2011-01
- Volume
- 144
- Issue
- 1
- Pages
- 79-91
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3062502
- OpenAlex
- W2023402149
- Cited by
- 1,059
- References
- 60
- Citations by year
- 2026: 54 · 2025: 52 · 2024: 80 · 2023: 58 · 2022: 82 · 2021: 78 · 2020: 70 · 2019: 62 · 2018: 74 · 2017: 59 · 2016: 82 · 2015: 73 · 2014: 88 · 2013: 62 · 2012: 60
- FWCI
- 26.93
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG024365)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- electron transport chain, longevity, aging, mitochondrial stress response, non-cell-autonomous signaling, Caenorhabditis elegans, mitochondrial function
- MeSH terms
- Aging, Animals, Electron Transport, Longevity, Mitochondria, Cellular Senescence, Caenorhabditis elegans, Oxidative Stress, Unfolded Protein Response
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