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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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“…implicated in neuro-development, brain metabolism, psychiatric disease, and neurodegeneration ( Balaraju et al., 2020 ; Chaouch et al., 2014 ; Edvardson et al., 2013 ; Gokhale et al., 2019 ; Akita et al., 2018 ; Lin-Hendel et al., 2016 ; Nota et al., 2013 ; Rigby et al., 2022 ; Siciliano et…”
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A single biochemical activity underlies the pleiotropy of the aging-related protein CLK-1
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“The transgenic strains generated for the study were: MQ1964 ukSi1 [pclk1::clk-1::gfp, cb-unc-119(+)]; clk-1(qm30), MQ1966 ukSi2 [pclk-1::clk-1 ΔMTS (13-187)::gfp, cb-unc-119(+)]; clk-1(qm30), MQ1993 ukSi2 [pclk-1::clk-1 ΔMTS (13-187)::gfp, cb-unc-119(+)]; clk-1(e2519), MQ1968 ukSi2 [pclk-1::clk-1 ΔMTS (13-187)::gfp, c…”
A comprehensive review on signaling attributes of serine and serine metabolism in health and disease
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Drosophila as a Model to Study the Link between Metabolism and Cancer
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“Accumulating evidence shows that mitochondrial alterations in one organ can have systemic effects through hormonal signalling [90,91].”
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“The UPR MT has been linked to the lifespan extension of clk-1 and isp-1 mit mutants and has been shown to be upregulated specifically in cco-1 RNAi (18).”
InfluentialInsights Into the Links Between Proteostasis and Aging From C. elegans
Zhang, W., Koyuncu, S., & Vílchez, D. (2022) · Frontiers in Aging · doi:10.3389/fragi.2022.854157 · Cited by 33
“These insights have been made possible through the use of C. elegans as a model organism, and although comparatively slower, these key findings are starting to be reproduced in mammalian models (Essers et al., 2016; Thompson et al., 2016; Swovick et al., 2021).”
BackgroundAccumulation of F-actin drives brain aging and limits healthspan in Drosophila
Schmid, E. T., Schinaman, J. M., Liu-Abramowicz, N., Williams, K. S., & Walker, D. W. (2024) · Nature Communications · doi:10.1038/s41467-024-53389-w · Cited by 35
“Previous work has shown that neuronal RNAi of electron transport chain (ETC) genes can prolong lifespan 68,69 .”
Curt, A., Zhang, J., Minnerly, J., & Jia, K. (2014) · Developmental & Comparative Immunology · doi:10.1016/j.dci.2014.03.009 · Cited by 32
Mechanisms by Which Different Functional States of Mitochondria Define Yeast Longevity
Beach, A., Leonov, A., Arlia‐Ciommo, A., Svistkova, V., Lutchman, V., & Titorenko, V. I. (2015) · International Journal of Molecular Sciences · doi:10.3390/ijms16035528 · Cited by 32
“to the nucleus to synthesize acetyl-CoA used for histone acetylation, S phase entry and cell-cycle progression [90]; and (6) mitokines in the nematode Caenorhabditis elegans; after these diffusible factors of unknown chemical nature exit mildly stressed mitochondria in neuronal cells, they act in an endocrine-like fas…”
BackgroundMitochondrial electron transport chain functions in long-lived Ames dwarf mice
Choksi, K. B., Nuss, J. E., DeFord, J. H., & Papaconstantinou, J. (2011) · Aging · doi:10.18632/aging.100357 · Cited by 32
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Chemical activation of a food deprivation signal extends lifespan
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“Moreover, the unfolded protein response of the endoplasmic reticulum (UPRER) and the mitochondria (UPRmito) is also influenced by neuronal function (Durieux et al., 2011; Sun et al., 2011; Singh & Aballay, 2012; Taylor & Dillin, 2013).”
BackgroundLetizia, M. C., Cornaglia, M., Trouillon, R., Sorrentino, V., Mouchiroud, L., Sleiman, M. S. B., Auwerx, J. H., & Gijs, M. A. M. (2018) · Microsystems & Nanoengineering · doi:10.1038/s41378-018-0003-8 · Cited by 30
The Role of Growth Differentiation Factor 15 in Energy Metabolism
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Mitochondrial control of cellular protein homeostasis
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Boosting mitochondrial health to counteract neurodegeneration
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BackgroundSilva, M. C., Amaral, M. D., & Morimoto, R. I. (2013) · PLoS Genetics · doi:10.1371/journal.pgen.1003711 · Cited by 33
“mitochondrial function, including the electron transport chain and the mitochondrial UPR, was shown to affect the rate of aging [27].”
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“High levels of mitochondrial stress can promote ROS production and reduce ATP synthesis (Woo and Shadel, 2011; Durieux et al., 2011).”
BackgroundShamalnasab, M., Gravel, S., St‐Pierre, J., Breton, L., Jäger, S., & Aguilaniu, H. (2018) · Aging Cell · doi:10.1111/acel.12830 · Cited by 32
Light stimulation of mitochondria reduces blood glucose levels
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The germline coordinates mitokine signaling
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“3 activity in the germline mediates UPR MT signaling between the neurons and UPR MT signaling, such as the neuron-specific knockdown of the mitochondrial complex IV subunit cco-1 (rab-3p::cco-1 hairpin in the sid-1(qt9) genetic background) 11 and found that the ucr-2.”
InfluentialIt's All in Your Mind: Determining Germ Cell Fate by Neuronal IRE-1 in C. elegans
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Improved mitochondrial stress response in long‐lived Snell dwarf mice
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“Follow‐up studies identified the upregulation of mtUPR as one mechanism linking mitochondrial changes to nematode lifes‐ pan extension (Durieux et al., 2011), which was further supported by the observation that overexpression of a single mtUPR gene (hsp70F) was sufficient to extend lifespan in C.…”
BackgroundKim, K. H. (2023) · Theranostics · doi:10.7150/thno.84165 · Cited by 33
Sensory systems: their impact on C. elegans survival
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“…of the unfolded protein response (UPR) in the endoplasmic reticulum (ER) of ASI neurons promotes dauer entry (Kulalert and Kim, 2013), whereas activation of UPR in the ER of all neurons (Taylor and Dillin, 2013) or in the mitochondria of downstream tissues (Durieux et al., 2011) promotes longevity.”
BackgroundEffect of mitochondrial stress on systemic metabolism
Lee, M. (2015) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.12822 · Cited by 32
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“…is usually divided into two components: extrinsic noise consists of variations due to cell-to-cell differences, such as ribosome copy number, whereas intrinsic noise is caused by the inherent randomness of the gene expression process (Elowitz et al., 2002; Fraser et al., 2004; Kærn et al., 2005).”
BackgroundUPRmt and coordinated UPRER in type 2 diabetes
Kang, Z., Chen, F., Wu, W., Liu, R. R., Chen, T., & Xu, F. (2022) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2022.974083 · Cited by 29
“The UPR is a mitochondrial stress response that maintains proteostasis in the mitochondria (Haynes and Ron, 2010; Schmidt et al., 2010; Durieux et al., 2011; Ott et al., 2016; Xie et al., 2017; Smyrnias et al., 2019).”
BackgroundImproved insulin sensitivity associated with reduced mitochondrial complex IV assembly and activity
Deepa, S. S., Pulliam, D. A., Hill, S., Shi, Y., Walsh, M. E., Salmon, A. B., Sloane, L. B., Zhang, N., Zeviani, M., Viscomi, C. F., et al. (2012) · The FASEB Journal · doi:10.1096/fj.12-221879 · Cited by 30
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Inter-tissue communication of mitochondrial stress and metabolic health
Zhang, H., Li, X., Fan, W., Pandovski, S., Tian, Y., & Dillin, A. G. (2023) · Life Metabolism · doi:10.1093/lifemeta/load001 · Cited by 30
“elegans since the first report of the cell non-autonomous nature of electron transport chain-mediated longevity [7].”
InfluentialThe mitochondrial integrated stress response: A novel approach to anti-aging and pro-longevity
Wang, X., & Zhang, G. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102603 · Cited by 29
“…are defects in mitochondrial DNA replication, nucleus-encoded mitochondrial protein defects, blockage of the electron transport chain (ETC), and mitochondrial dynamics dysfunction (Chung et al., 2017; Durieux et al., 2011; Forsstrom et al., 2019; Khan et al., 2017; Quiros et al., 2017) (Fig.”
Mitochondria in aging and age-associated diseases
Pahal, S., Mainali, N., Balasubramaniam, M., Reis, R. J. S., & Ayyadevara, S. (2025) · Mitochondrion · doi:10.1016/j.mito.2025.102022 · Cited by 32
The Intestine as a Lifespan- and Proteostasis-Promoting Signaling Tissue
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“elegans as well as vertebrate models (Bishop and Guarente, 2007; Durieux et al., 2011; Taylor and Dillin, 2013; Williams et al., 2014; Shao et al., 2016), opening new questions on the exact neural circuits orchestrating organismal proteostasis.”
BackgroundInfluentialAutophagy activation can partially rescue proteasome dysfunction‐mediated cardiac toxicity
Papanagnou, E., Gumeni, S., Sklirou, A. D., Rafeletou, A., Terpos, E., Keklikoglou, K., Kastritis, E., Stamatelopoulos, K. S., Sykiotis, G. P., Dimopoulos, M. A., et al. (2022) · Aging Cell · doi:10.1111/acel.13715 · Cited by 32
“Similarly, unfolded protein stress in different cellular compartments of the neuron, for example, cytoplasm (Prahlad et al., 2008), mitochondria (Durieux et al., 2011), or the ER (Taylor & Dillin, 2013) transmit the respective stress responses to distal tissues, while expression of an aggregation-…”
BackgroundComparative Endocrinology of Aging and Longevity Regulation
Allard, J. B., & Duan, C. (2011) · Frontiers in Endocrinology · doi:10.3389/fendo.2011.00075 · Cited by 30
“A mutation which alters mitochondrial function can extend lifespan even when present only in certain cells, indicating cell-non-autonomous functions even for a mutation affecting a fundamental metabolic process (Durieux et al., 2011).”
BackgroundInter-organ signalling by HRG-7 promotes systemic haem homeostasis
Sinclair, J. W., Pinter, K. L., Samuel, T. K., Beardsley, S., Yuan, X., Zhang, J., Meng, K., Yun, S., Krause, M., & Hamza, I. (2017) · Nature Cell Biology · doi:10.1038/ncb3539 · Cited by 29
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“For instance, worms with a reduced OXPHOS function in neurons have a prolonged lifespan due to the activation of UPRmt in intestinal cells through a cell non-autonomous manner (Durieux et al., 2011).”
BackgroundRegulation of proteostasis and innate immunity via mitochondria-nuclear communication
Kim, S., Ramalho, T. R. D. O., & Haynes, C. M. (2024) · The Journal of Cell Biology · doi:10.1083/jcb.202310005 · Cited by 30
“…elegans demonstrated that mitochondrial perturbations caused by polyglutamine expression within neurons resulted in mitochondrial stress and UPR mt activation in neurons as well as in intestinal cells, which promotes lifespan extension (Durieux et al., 2011) (reviewed here [Zhang et al., 2023a]).”
BackgroundMammalian mitohormesis: from mitochondrial stressors to organismal benefits
Gunawan, A. L., Liparulo, I., & Stahl, A. (2025) · The EMBO Journal · doi:10.1038/s44318-025-00549-3 · Cited by 33
“(12) 2011: Cell non-autonomous mitohormetic mechanisms are discovered in C. elegans (Durieux et al, 2011).”
Double-edged alliance: mitochondrial surveillance by the UPS and autophagy
Franz, A., Kevei, É., & Hoppe, T. (2015) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2015.08.004 · Cited by 29
“Interestingly, mitochondrial dysfunction in a defined tissue is capable of initiating this systemic response in distal tissues in C. elegans and Drosophila [72], [73].”
Meta-analysis of global metabolomic data identifies metabolites associated with life-span extension
Patti, G. J., Tautenhahn, R., Johannsen, D. L., Kalisiak, E., Ravussin, É., Brüning, J. C., Dillin, A. G., & Siuzdak, G. E. (2013) · Metabolomics · doi:10.1007/s11306-013-0608-8 · Cited by 28
“…known to affect life span in a cell-non-autonomous nature, suggesting that molecular signals from specific tissues distally regulate aging of the whole organism (Arantes-Oliveira et al. 2002; Broughton et al. 2005; Durieux et al. 2011; Hwangbo et al. 2004; Libina et al. 2003; Wolkow et al. 2000).”
BackgroundFibroblast growth factor 21 and autophagy: A complex interplay in Parkinson disease
Kakoty, V., Sarathlal, K. C., Tang, R.-D., Yang, C. H., Dubey, S. K., & Taliyan, R. (2020) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2020.110145 · Cited by 27
Regulation of the lysosome by sphingolipids: Potential role in aging
Tang, H., Huang, X., & Pang, S. (2022) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2022.102118 · Cited by 26
Higashitani, A., Teranishi, M., Nakagawa, Y., Itoh, Y., Sudevan, S., Szewczyk, N. J., Kubota, Y., Abe, T., & Kobayashi, T. (2023) · The FASEB Journal · doi:10.1096/fj.202201489rr · Cited by 27
Kulalert, W., & Kim, D. H. (2013) · Current Biology · doi:10.1016/j.cub.2013.10.058 · Cited by 29
Mitochondria: Masters of Epigenetics
Tatar, M., & Sedivy, J. M. (2016) · Cell · doi:10.1016/j.cell.2016.05.021 · Cited by 29
Guha, S., Mathew, N. D., Konkwo, C., Ostrovsky, J., Kwon, Y. J., Polyák, E., Seiler, C., Bennett, M. J., Xiao, R., Zhang, Z., et al. (2021) · Human Molecular Genetics · doi:10.1093/hmg/ddab059 · Cited by 29
“…in C. elegans leads to transcriptional upregulation of mitochondrial chaperone proteins hsp-6 and hsp-60 , as has been shown by GFP reporter studies following knockdown of electron transport chain components or when mitochondrial stress is present by the L3/L4 larval stage transition (25).”
Ruparelia, A. A., Salavaty, A., Barlow, C. K., Lu, Y., Sonntag, C., Hersey, L., Eramo, M. J., Krug, J., Reuter, H., Schittenhelm, R. B., et al. (2023) · Aging Cell · doi:10.1111/acel.13862 · Cited by 28
“…complexes following genetic and/or pharmacological manipulations has also been shown to trigger ROS-mediated mito-hormesis and extend life span in multiple organisms including killifish (Baumgart et al., 2016 ; Copeland et al., 2009 ; Durieux et al., 2011; Feng et al., 2001 ; Lee et al., 2002 ).”
BackgroundA feedback loop governs the relationship between lipid metabolism and longevity
Littlejohn, N. K., Seban, N., Liu, C., & Srinivasan, S. (2020) · eLife · doi:10.7554/elife.58815 · Cited by 27
Exercise, Mitohormesis, and Mitochondrial ORF of the 12S rRNA Type-C (MOTS-c)
Yoon, T. K., Lee, C. H., Kwon, O., & Kim, M. (2022) · Diabetes & Metabolism Journal · doi:10.4093/dmj.2022.0092 · Cited by 28
Gildea, H. K., Frankino, P. A., Tronnes, S. U., Pender, C. L., Durieux, J., Dishart, J. G., Choi, H. O., Hunter, T. D., Cheung, S. S., Frakes, A. E., et al. (2022) · Science Advances · doi:10.1126/sciadv.abq3970 · Cited by 27
Jafari, G., Wasko, B. M., Tonge, A., Schurman, N., Dong, C., Li, Z., Peters, R., Kayser, E., Pitt, J. N., Morgan, P. G., et al. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1509416112 · Cited by 27
Li, G., Gong, J., Liu, J., Liu, J., Li, H., Hsu, A., Liu, J., & Xu, X. Z. S. (2019) · Science Advances · doi:10.1126/sciadv.aau5041 · Cited by 27
Tong, D., Zhang, D., Fei, X., Teng, M., Jiang, X., Hou, J., Zhang, Q., & Huang, Y. (2012) · Pharmacology · doi:10.1159/000338628 · Cited by 27
Jazwinski, S. M. (2014) · Ageing Research Reviews · doi:10.1016/j.arr.2014.12.007 · Cited by 26
Horan, M. P., Gemmell, N. J., & Wolff, J. N. (2013) · European Journal of Human Genetics · doi:10.1038/ejhg.2013.75 · Cited by 26
Raman, P., Zaghab, S. M., Traver, E. C., & Jose, A. M. (2017) · Nucleic Acids Research · doi:10.1093/nar/gkx484 · Cited by 27
Dahlmans, D., Houzelle, A., Andreux, P. A., Wang, X., Jörgensen, J. A., Moullan, N., Daemen, S., Kersten, S., Auwerx, J. H., & Hoeks, J. (2018) · Journal of Cellular Physiology · doi:10.1002/jcp.27401 · Cited by 27
“…demonstrated that activation of the mtUPR through cco‐1 (a nuclear encoded subunit of the ETC) and spg‐7 (a mitochondrial protein quality control protease) loss of function, activated the mtUPR and increased lifespan in C. elegans (Durieux et al., 2011; Wu et al., 2014; Yoneda et al., 2004).”
BackgroundSolid-phase inclusion as a mechanism for regulating unfolded proteins in the mitochondrial matrix
Ruan, L., McNamara, J. T., Zhang, X., Chang, A. C.-C., Zhu, J., Dong, Y., Sun, G. L., Peterson, A. F., Na, C. H., & Li, R. (2020) · Science Advances · doi:10.1126/sciadv.abc7288 · Cited by 24
Organismal and Cellular Stress Responses upon Disruption of Mitochondrial Lonp1 Protease
Taouktsi, E., Kyriakou, E., Smyrniotis, S., Borbolis, F., Bondi, L., Avgeris, S. N., Trigazis, E., Rigas, S., Voutsinas, G. E., & Syntichaki, P. (2022) · Cells · doi:10.3390/cells11081363 · Cited by 28
Targeting Mitochondria to Control Ageing and Senescence
Protasoni, M., & Serrano, M. (2023) · Pharmaceutics · doi:10.3390/pharmaceutics15020352 · Cited by 30
“Indeed, UPRmt triggering after exposure to mitochondrial stress shows strong responses only during development [102,103], while it appears less active in later stages of life when there is no reported increased lifespan as a response to stressors [96,104,105].”
BackgroundMitochondrial-Mimicking Nanozyme-Catalyzed Cascade Reactions for Aging Attenuation
Cong, W., Li, M., Pan, Y., Wang, H., Zhu, J., Huang, Y., & Huang, Q. (2022) · Nano Today · doi:10.1016/j.nantod.2023.101757 · Cited by 26
Shamalnasab, M., Dhaoui, M., Thondamal, M., Harvald, E. B., Færgeman, N. J., Aguilaniu, H., & Fabrizio, P. (2017) · Aging · doi:10.18632/aging.101267 · Cited by 26
Metolazone upregulates mitochondrial chaperones and extends lifespan in Caenorhabditis elegans
Ito, A., Zhao, Q., Tanaka, Y., Yasui, M., Katayama, R., Sun, S., Tanimoto, Y., Nishikawa, Y., & Kage‐Nakadai, E. (2020) · Biogerontology · doi:10.1007/s10522-020-09907-6 · Cited by 24
HSF-1: Guardian of the Proteome Through Integration of Longevity Signals to the Proteostatic Network
Lázaro‐Peña, M. I., Ward, Z. C., Yang, S., Strohm, A. O., Merrill, A. K., Soto, C. A., & Samuelson, A. V. (2022) · Frontiers in Aging · doi:10.3389/fragi.2022.861686 · Cited by 27
Pyruvate dehydrogenase complex (PDC) export from the mitochondrial matrix
Ng, F., & Tang, B. L. (2014) · Molecular Membrane Biology · doi:10.3109/09687688.2014.987183 · Cited by 25
“Mitochondrial-based UPRmt and retrograde signaling could well be mediated, at least in Caenorhabditis elegans, in a non-cell autonomous manner (Durieux et al., 2011) by mitochondrial signals of unknown molecular nature known as mitokines (Long et al., 2014).”
BackgroundHur, J. H., Stork, D. A., & Walker, D. W. (2014) · Journal of Bioenergetics and Biomembranes · doi:10.1007/s10863-014-9553-0 · Cited by 27
“These stress response mechanisms, such as the mitochondrial unfolded protein response (mitoUPR) have been shown to be important for the extended lifespans in studies of knock down of certain ETC genes (OwusuAnsah et al. 2013; Houtkooper et al. 2013; Durieux et al. 2011).”
Mitochondrial deficiency: a double-edged sword for aging and neurodegeneration
Troulinaki, K., & Bano, D. (2012) · Frontiers in Genetics · doi:10.3389/fgene.2012.00244 · Cited by 24
“Even when restricted to a single tissue, like the intestine or the nervous system, mitochondrial dysfunction can extend the lifespan of the whole organism (Durieux et al., 2011).”
BackgroundMitochondrial function and regulation of macrophage sterol metabolism and inflammatory responses
Graham, A. (2015) · World Journal of Cardiology · doi:10.4330/wjc.v7.i5.277 · Cited by 24
Jiang, J. C., Stumpferl, S. W., Tiwari, A., Qin, Q., Rodríguez-Quiñones, J. F., & Jazwinski, S. M. (2016) · Genetics · doi:10.1534/genetics.116.188086 · Cited by 24
“…in tissue culture (Dell’agnello et al. 2007; Passos et al. 2007; Caldeira da Silva et al. 2008; Lapointe and Hekimi 2008; Copeland et al. 2009; Lee et al. 2010; Yang and Hekimi 2010; Durieux et al. 2011; Liu et al. 2011; Walter et al. 2011; Liu et al. 2012; Jazwinski 2015; Mishur et al. 2016).”
BackgroundRegulation of cell-non-autonomous proteostasis in metazoans
O'Brien, D., & van Oosten‐Hawle, P. (2016) · Essays in Biochemistry · doi:10.1042/ebc20160006 · Cited by 23
Lebeau, J., Rainbolt, T. K., & Wiseman, R. L. (2018) · International review of cytology · doi:10.1016/bs.ircmb.2018.05.003 · Cited by 25
“, 2013), and alterations in mitochondrial co-factor levels (Baker et al., 2012a; Durieux et al., 2011).”
BackgroundWhen is Sirt1 activity bad for dying neurons?
Ng, F., & Tang, B. L. (2013) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2013.00186 · Cited by 24
“Furthermore, manipulation of respiratory function of neurons appears to generate, in a non-cell autonomous manner, mitochondrial stress response in other tissues that enhanced survival (Durieux et al., 2011).”
BackgroundGenes and Pathways That Influence Longevity in Caenorhabditis elegans
Lee, Y., An, S. W. A., Artan, M., Seo, M., Hwang, A. B., Jeong, D., Son, H. G., Hwang, W., Lee, D.-Y., Seo, K., et al. (2015) · Springer eBooks · doi:10.1007/978-4-431-55763-0_8 · Cited by 24
C. elegans screening strategies to identify pro-longevity interventions
Maglioni, S., Arsalan, N., & Ventura, N. (2016) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2016.07.010 · Cited by 25
Hua, X., & Wang, D. (2025) · Journal of environmental chemical engineering · doi:10.1016/j.jece.2025.116571 · Cited by 23
Quality control in mitochondria: use it, break it, fix it, trash it
Kornmann, B. (2014) · F1000Prime Reports · doi:10.12703/p6-15 · Cited by 26
“In a screen for long-lived worm mutants, Andrew Dillin’s lab found that creating imbalance in the assembly of respiratory chain subunits caused increased lifespan [3].”
BackgroundLove is a battlefield: programmed cell death during fertilization
Heydlauff, J., & Groß‐Hardt, R. (2014) · Journal of Experimental Botany · doi:10.1093/jxb/eru030 · Cited by 23
“As a matter of fact, Durieux et al. (2011) report that artificial electron transport chain impairment in neurons of Caenorhabditis elegans is communicated to the intestine where the mitochondria-specific unfolded protein response is activated, resulting in an extended lifespan.”
BackgroundInhibition of elongin C promotes longevity and protein homeostasis via HIF ‐1 in C. elegans
Hwang, W., Artan, M., Seo, M., Lee, D.-Y., Nam, H. G., & Lee, S. (2015) · Aging Cell · doi:10.1111/acel.12390 · Cited by 23
“Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. components (Durieux et al., 2011; Walter et al., 2011; Baruah et al., 2014), because nhr-57 is induced by impaired mitochondrial functions (Lee et al., 2010).”
BackgroundC. elegans miro-1 Mutation Reduces the Amount of Mitochondria and Extends Life Span
Yanqing, S., Ng, L. F., Low, N. P. W., Hagen, T., Gruber, J., & Inoue, T. (2016) · PLoS ONE · doi:10.1371/journal.pone.0153233 · Cited by 23
“In particular, activation of the mitochondrial unfolded protein response pathway has been proposed to underlie lifespan extension in some ETC mutants [16, 17].”
Mitochondrial stress and aging: Lessons from C. elegans
Chen, P. X., Zhang, L., Chen, D., & Tian, Y. (2023) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2023.02.010 · Cited by 23
Tower, J., Landis, G. N., Gao, R. W., Luan, A., Lee, J., & Sun, Y. (2013) · The Journals of Gerontology Series A · doi:10.1093/gerona/glt078 · Cited by 24
Mitochondrial Dysfunction in Cardiorenal Syndrome
Doi, K., & Noiri, E. (2016) · Antioxidants and Redox Signaling · doi:10.1089/ars.2016.6654 · Cited by 24
“One basic study demonstrated that mitochondrial dysfunction in the brain of Caenorhabditis elegans induced the mitochondrial unfolded protein response (UPR mt ) in a distant organ of intestine, although no secreted factor was defined yet (24).”
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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