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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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BackgroundInfluentialCell non-autonomous control of autophagy and metabolism by glial cells
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Translational regulation in stress biology
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Restoring stem cells — all you need is NAD+
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ASI-RIM neuronal axis regulates systemic mitochondrial stress response via TGF-β signaling cascade
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“For instance, knocking down the mitochondrial electron transport chain (ETC) component cco-1 in neurons activates the mitochondrial unfolded protein response (UPR mt ) in the intestine, extending lifespan 3 .”
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Anterograde regulation of mitochondrial genes and FGF21 signaling by hepatic LSD1
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Mitochondrial protein import and UPRmt in skeletal muscle remodeling and adaptation
Richards, B. J., Slavin, M. B., Oliveira, A. N., Sanfrancesco, V. C., & Hood, D. A. (2022) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2022.01.002 · Cited by 19
Cell Non-autonomous Proteostasis Regulation in Aging and Disease
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“Depletion of cco-1 in the whole organism leads to the same increase in the lifespan in the worm (Durieux et al., 2011).”
BackgroundInfluentialEnhancing mitochondrial proteolysis alleviates alpha-synuclein-mediated cellular toxicity
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A germline-to-soma signal triggers an age-related decline of mitochondrial stress response
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“In particular, the life-span extension that results from dysfunctional mitochondria often requires intact mitochondrial stress responses ( 17 , 18 , 30 – 33 ).”
Chiariello, A., Rossetti, L. M., Valente, S., Pasquinelli, G., Sollazzo, M., Iommarini, L., Porcelli, A. M., Tognocchi, M., Conte, G., Santoro, A., et al. (2024) · Aging Cell · doi:10.1111/acel.14111 · Cited by 17
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“47 In a similar vein, depletion of the mitochondrial complex IV assembly protein Surf1 results in UPR mt activation, enhancing resistance to oxidative stress-induced cell death.”
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Mitochondrial Physiology of Cellular Redox Regulations
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“The latter exists with the metabokine/mitokine signaling [133-135], mt-nuclear crosstalk [136-139], and mt-initiated epigenome remodeling [140-143].”
BackgroundDifferent roles of circulating and intramuscular GDF15 as markers of skeletal muscle health
Chiariello, A., Conte, G., Rossetti, L. M., Trofarello, L., Salvioli, S., & Conte, M. (2024) · Frontiers in Endocrinology · doi:10.3389/fendo.2024.1404047 · Cited by 17
GLTSCR2/PICT1 links mitochondrial stress and Myc signaling
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“elegans, the mitochondrial unfolded protein signaling is apparently required for the lifespan-extending effect of electron transport chain defects in that organism (31).”
BackgroundMitochondrial ubiquinone–mediated longevity is marked by reduced cytoplasmic mRNA translation
Molenaars, M., Janssens, G. E., Santermans, T., Lezzerini, M., Jelier, R., MacInnes, A. W., & Houtkooper, R. H. (2018) · Life Science Alliance · doi:10.26508/lsa.201800082 · Cited by 15
“…in the TE of mRNAs coding for the translation machinery is highly reminiscent of the proteomic landscape we described in the daf-2 mutants, where there is a scarcity of ribosomal proteins (RPs) yet also no appreciable reduction in total RP mRNA expression (Depuydt et al, 2013; Essers et al, 2015).”
BackgroundResultInfluentialAtakan, H. B., Cornaglia, M., Mouchiroud, L., Auwerx, J. H., & Gijs, M. A. M. (2018) · Lab on a Chip · doi:10.1039/c8lc00863a · Cited by 17
Neuronal AMPK coordinates mitochondrial energy sensing and hypoxia resistance in C. elegans
Berry, B. J., Baldzizhar, A., Nieves, T., & Wojtovich, A. P. (2020) · The FASEB Journal · doi:10.1096/fj.202001150rr · Cited by 16
The disposable soma theory of aging in reverse
Douglas, P. M., & Dillin, A. G. (2013) · Cell Research · doi:10.1038/cr.2013.148 · Cited by 19
Mahapatra, G., Smith, S. C., Hughes, T. M., Wagner, B., Maldjian, J. A., Freedman, B. I., & Molina, A. J. A. (2018) · Clinical Science · doi:10.1042/cs20180690 · Cited by 16
Mitochondrial Unfolded Protein Response and Its Roles in Stem Cells
Shen, G., Liu, W., Xu, L., & Wang, L. (2020) · Stem Cells and Development · doi:10.1089/scd.2019.0278 · Cited by 17
“As previously mentioned, mild activation of the UPR mt promotes longevity and has its potential ability to delay senescence [18,41,42].”
InfluentialCollaboration between mitochondria and the nucleus is key to long life in Caenorhabditis elegans
Chang, H.-W., Shtessel, L., & Lee, S. S. (2015) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2014.10.576 · Cited by 15
“effects, this signal does not rely on UBL-5, which appears to function exclusively in a cellautonomous manner in the intestine [72].”
InfluentialSenchuk, M. M., Raamsdonk, J. M. V., & Moore, D. J. (2021) · Neurobiology of Disease · doi:10.1016/j.nbd.2021.105267 · Cited by 16
Zhao, Q., Rangan, R., Weng, S., Özdemir, C., & Cenik, E. S. (2023) · PLoS Biology · doi:10.1371/journal.pbio.3002276 · Cited by 14
Bacteria–organelle communication in physiology and disease
Lee, Y.-T., Şentürk, M., Guan, Y., & Wang, M. C. (2024) · The Journal of Cell Biology · doi:10.1083/jcb.202310134 · Cited by 15
“This revelation aligns with the understanding that mitochondria themselves have a bacterial ancestry and actively participate in the regulation of lifespan through cell non-autonomous communication between tissues (Durieux et al., 2011).”
BackgroundMitochondria – the CEO of the cell
Lee-Glover, L. P., Picard, M. A., & Shutt, T. E. (2025) · Journal of Cell Science · doi:10.1242/jcs.263403 · Cited by 16
Wu, J., Yarmey, V. R., Yang, O. J., Soderblom, E. J., San‐Miguel, A., & Yan, D. (2025) · Nature Neuroscience · doi:10.1038/s41593-025-01989-0 · Cited by 16
Molecular characterization of the transition to mid-life in Caenorhabditis elegans
Eckley, D. M., Rahimi, S., Mantilla, S., Orlov, N. V., Coletta, C. E., Wilson, M. A., Iser, W. B., Delaney, J. D., Zhang, Y., Wood, W. H., et al. (2012) · AGE · doi:10.1007/s11357-012-9401-2 · Cited by 14
“A recent study (Durieux et al. 2011) showed that mitochondrial signals from neurons can affect the organism's lifespan through their action in the intestine.”
BackgroundSelective manipulation of aging: a novel strategy for the treatment of neurodegenerative disorders
Cohen, E., Moll, L., & Elami, T. (2014) · Swiss Medical Weekly · doi:10.4414/smw.2014.13917 · Cited by 15
Mao, C.-C., & Cai, X. (2020) · Current Stem Cell Research & Therapy · doi:10.2174/1574888x15666200422103916 · Cited by 16
Both objective and paradoxical insomnia elicit a stress response involving mitokine production
Martucci, M., Conte, M., Ostan, R., Chiariello, A., Miele, F., Franceschi, C., Salvioli, S., Santoro, A., & Provini, F. (2020) · Aging · doi:10.18632/aging.103274 · Cited by 15
Kuzuoğlu‐Öztürk, D., Hu, Z., Rama, M., Devericks, E. N., Weiss, J., Chiang, G. G., Worland, S. T., Brenner, S. E., Goodarzi, H., Gilbert, L. A., et al. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.109321 · Cited by 16
“The UPR mt was first described in mammals (Martinus et al., 1996; Zhao et al., 2002) and then further characterized in C. elegans where it extends lifespan (Durieux et al., 2011; Houtkooper et al., 2013, Shpilka and Haynes, 2018).”
Moehle, E. A., Higuchi‐Sanabria, R., Tsui, C. K., Homentcovschi, S., Tharp, K. M., Zhang, H., Chi, H. M., Joe, L. K., Rogers, M. D. L. R., Sahay, A., et al. (2021) · Science Advances · doi:10.1126/sciadv.abj6818 · Cited by 13
“1, A and B, and see Materials and Methods for details).”
BackgroundInfluentialAging: Seeking Mitonuclear Balance
Karpac, J., & Jasper, H. (2013) · Cell · doi:10.1016/j.cell.2013.06.046 · Cited by 15
“These stress responses include both the mitochondrial unfolded protein response (UPRmt; Durieux et al., 2011) and mitochondrial ROSinduced defense pathways (mitohormesis response; Lee et al., 2010; Schulz et al., 2007).”
BackgroundHaeussler, S., Yeroslaviz, A., Rolland, S. G. M., Luehr, S., Lambie, E. J., & Conradt, B. (2021) · G3 Genes Genomes Genetics · doi:10.1093/g3journal/jkab095 · Cited by 12
“…elegans interactomes were compiled for FZO-1 or all 16 genes that are currently associated with the GO-term ‘mitochondrial unfolded protein response’ (GO:0034514) from scientific literature (Durinck et al., 2009; Simonis et al., 2009) and databases such as mentha (Calderone et al., 2013), BioGRID3.”
MethodChu, X., Subramani, K., Thomas, B., Terry, A. V., Fulzele, S., & Raju, R. P. (2022) · Aging and Disease · doi:10.14336/ad.2021.0830 · Cited by 14
Surveying Low-Cost Methods to Measure Lifespan and Healthspan in Caenorhabditis elegans
Torres, T. C., Moaddeli, D., Averbukh, M., Coakley, A. J., Dutta, N., Garcia, G., & Higuchi‐Sanabria, R. (2022) · Journal of Visualized Experiments · doi:10.3791/64091 · Cited by 14
Riboflavin depletion promotes longevity and metabolic hormesis in Caenorhabditis elegans
Yerevanian, A. I., Murphy, L., Emans, S. W., Zhou, Y., Ahsan, F. M., Baker, D. J., Li, S., Adedoja, A., Cedillo, L., Stuhr, N. L., et al. (2022) · Aging Cell · doi:10.1111/acel.13718 · Cited by 13
Neuron-periphery mitochondrial stress communication in aging and diseases
Li, J., Cui, J., & Tian, Y. (2022) · Life Medicine · doi:10.1093/lifemedi/lnac051 · Cited by 14
Mitochondrial-derived peptides: Antidiabetic functions and evolutionary perspectives
Kal, S., Mahata, S., Jati, S., & Mahata, S. K. (2023) · Peptides · doi:10.1016/j.peptides.2023.171147 · Cited by 15
Reproductive regulation of the mitochondrial stress response in Caenorhabditis elegans
Charmpilas, N., Sotiriou, A., Axarlis, K., Tavernarakis, N., & Hoppe, T. (2024) · Cell Reports · doi:10.1016/j.celrep.2024.114336 · Cited by 15
Olfaction regulates peripheral mitophagy and mitochondrial function
Dishart, J. G., Pender, C. L., Shen, K., Zhang, H., Ly, M., Webb, M., & Dillin, A. G. (2024) · Science Advances · doi:10.1126/sciadv.adn0014 · Cited by 12
Mitonuclear Communication in Stem Cell Function
Peng, B., Wang, Y., & Zhang, H. (2024) · Cell Proliferation · doi:10.1111/cpr.13796 · Cited by 14
Septic Shock and the Aging Process: A Molecular Comparison
da Silva, F. P., & Machado, M. C. C. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.01389 · Cited by 14
“Indeed, mitochondria are important organelles in the maintenance of stem cells (12), the activation of the unfolded protein response (34), the regulation of innate and adaptive immune pathways (35, 36), and the modulation of the metabolic profile of the cell (32).”
BackgroundMessina, F., Cecconi, F., & Rodolfo, C. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.00271 · Cited by 14
“In this scenario, the increasing knowledge about this interplay could be beneficial to the development of combined therapeutic approaches, aiming to different aspects such as, ROS formation targeting, mitochondrial biogenesis stimulation, mitochondrial dynamics modulation (Elfawy and Das, 2019).”
BackgroundMitohormesis; Potential implications in neurodegenerative diseases
Gohel, D., & Singh, R. K. (2020) · Mitochondrion · doi:10.1016/j.mito.2020.11.011 · Cited by 14
Invertebrates Mitochondrial Function and Energetic Challenges
Martínez‐Cruz, O., Sánchez‐Paz, A., García-Carreño, F. L., Jiménez-Gutiérrez, L. R., del Toro, M. Á. N., & Muhlia‐Almazán, A. (2012) · InTech eBooks · doi:10.5772/32309 · Cited by 14
“Thus, it has been suggested that mitochondria may influence the longevity of the nematode Caenorhabditis elegans through the rate of ROS production and by the stress-evoked signals that are known to act in a cell-non-autonomous manner during mitochondrial protein regulation (Durieux et al., 2011).”
BackgroundRegulation of Age-related Decline by Transcription Factors and Their Crosstalk with the Epigenome
Zhou, X., Sen, I., Lin, X.-X., & Riedel, C. G. (2018) · Current Genomics · doi:10.2174/1389202919666180503125850 · Cited by 15
“elegans mutants with moderate mitochondrial dysfunction often display a longer lifespan [146-149].”
BackgroundA virus-acquired host cytokine controls systemic aging by antagonizing apoptosis
Mlih, M., Khericha, M., Birdwell, C. E., West, A. P., & Karpac, J. (2018) · PLoS Biology · doi:10.1371/journal.pbio.2005796 · Cited by 16
Zhang, M., Weng, H., & Zheng, J. (2019) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2019.105635 · Cited by 14
Miyata, Y., & Shimomura, I. (2013) · Journal of Diabetes Investigation · doi:10.1111/jdi.12064 · Cited by 13
Mitohormesis and mitochondrial dynamics in the regulation of stem cell fate
Barzegari, A., Aboulhassanzadeh, S., Landon, R., Gueguen, V., Meddahi‐Pellé, A., Parvizpour, S., Anagnostou, F., & Pavon‐Djavid, G. (2022) · Journal of Cellular Physiology · doi:10.1002/jcp.30820 · Cited by 14
“The concept of mitokines as cell‐nonautonomous mediators of mitochondrial stress has first been defined based on research in C. elegans (Durieux et al., 2011).”
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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