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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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Lionaki, E., Gkikas, I., & Tavernarakis, N. (2016) · Frontiers in Genetics · doi:10.3389/fgene.2016.00162 · Cited by 51
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Divergent Nodes of Non-autonomous UPRER Signaling through Serotonergic and Dopaminergic Neurons
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BackgroundUNC ‐120/ SRF independently controls muscle aging and lifespan in Caenorhabditis elegans
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“In light of these findings, it seems surprising that mild mitochondrial stress caused by targeted ablation of a mitochondrial ribosomal gene and the subsequent induction of UPR mt induction is reported to benefit longevity in various organisms (39–41).”
BackgroundGlial-derived mitochondrial signals affect neuronal proteostasis and aging
Bar‐Ziv, R., Dutta, N., Hruby, A. J., Sukarto, E., Averbukh, M., Alcala, A., Henderson, H. R., Durieux, J., Tronnes, S. U., Ahmad, Q., et al. (2023) · Science Advances · doi:10.1126/sciadv.adi1411 · Cited by 46
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van Oosten‐Hawle, P., & Morimoto, R. I. (2013) · Journal of Experimental Biology · doi:10.1242/jeb.091249 · Cited by 47
“Although these cellular stress responses have been thought to be induced in a strict cell-autonomous manner, recent advances now demonstrate that the cytoplasmic HSR, the UPRER and the UPRmt are all regulated by cell non-autonomous control in Caenorhabditis elegans, as will be discussed in the following sections.”
BackgroundInfluentialDroujinine, I. A., & Perrimon, N. (2013) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2013.00082 · Cited by 48
“In addition, tissue-specific induction of mitochondrial (Durieux et al., 2011), cytoplasmic (van Oosten-Hawle et al., 2013), Frontiers in Cellular and Infection Microbiology www.frontiersin.org November 2013 | Volume 3 | Article 82 | 1 CELLULAR AND INFECTION MICROBIOLOGY FIGURE 1 | Overview of the…”
BackgroundInfluentialActivation of the stress proteome as a mechanism for small molecule therapeutics
Brose, R. D., Shin, G., McGuinness, M. C., Schneidereith, T., Purvis, S. H., Dong, G.-X., Keefer, J. R., Spencer, F. A., & Smith, K. D. (2012) · Human Molecular Genetics · doi:10.1093/hmg/dds247 · Cited by 45
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BackgroundCombating neurodegenerative disease with chemical probes and model systems
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Molecular insights into the transgenerational inheritance of stress memory
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Initiation of innate immune responses by surveillance of homeostasis perturbations
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“…reports have revealed a novel connection between the sphingolipid biosynthesis and the endoplasmic reticulum UPR activation (Spassieva et al., 2009; Lépine et al., 2011; Epstein et al., 2012), but none was about the correlations between induction of UPRmt and the ceramide synthesis pathway in AD.”
BackgroundHumanin and Its Pathophysiological Roles in Aging: A Systematic Review
Coradduzza, D., Congiargiu, A., Chen, Z., Cruciani, S., Zinellu, A., Carru, C., & Medici, S. (2023) · Biology · doi:10.3390/biology12040558 · Cited by 46
“Mild mitochondrial stress would increase the resistance and survival of the entire organism, not only limited to the affected tissue or cell, but also spread to distal areas [75], due to increased ROS formation, which, in turn, activates a retrograde stress-resistance response culminating in lifespan extension.”
BackgroundMitochondrial membrane lipidome defines yeast longevity
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“A body of recent evidence supports the notion that the competence of mitochondria at performing the aforementioned three types of longevity-defining processes early in life of an eukaryotic organism or in a replicatively and chronologically “young” eukaryotic cell defines the long-term viability of the organism and th…”
BackgroundMitochondrial form, function and signalling in aging
Amigo, I., da Cunha, F. M., Forni, M. F., Garcia-Neto, W., Kakimoto, P. A., Luévano‐Martínez, L. A., Macedo, F. P., Menezes‐Filho, S. L., Peloggia, J., & Kowaltowski, A. J. (2016) · Biochemical Journal · doi:10.1042/bcj20160451 · Cited by 42
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Olfactory chemosensation extends lifespan through TGF-β signaling and UPR activation
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“Interestingly, the reduction of the mitochondrial metabolism by Hsp22 is also supported by preliminary data from our lab that show the down-regulation of multiple isoforms of proteins from the ETC and Krebs cycle among others upon Hsp22 over-expression (Morrow et al., submitted).”
BackgroundEndocrine aspects of organelle stress — cell non-autonomous signaling of mitochondria and the ER
Schinzel, R. T., & Dillin, A. G. (2015) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2015.01.006 · Cited by 42
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MOTS-c, the Most Recent Mitochondrial Derived Peptide in Human Aging and Age-Related Diseases
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The expression pattern of GDF15 in human brain changes during aging and in Alzheimer’s disease
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“, a soluble molecule produced and secreted in response to mitochondrial stress and able to induce an adaptive response also in distant cells not directly affected by the stressful agent (Durieux et al., 2011; Conte et al., 2020a).”
BackgroundStaab, T. A., Egrafov, O., Knowles, J. A., & Sieburth, D. (2014) · PLoS Genetics · doi:10.1371/journal.pgen.1004100 · Cited by 44
“How might increased expression of a synaptic cell adhesion molecule promote organismal survival in response to stress? Recent work has established the presence of ‘‘mitokines’’ in neurons—a signal produced in the neurons in response to dysfunctional mitochondrial electron transport [57]; release of these mitokines res…”
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“The induction of the mitochondrial unfolded protein response (UPR) initially emerged as of great importance for pro-longevity cues produced by long-lived mitochondrial mutants [21,22].”
Bhaskaran, S., Unnikrishnan, A., Ranjit, R., Qaisar, R., Pharaoh, G. A., Matyi, S., Kinter, M. T., & Deepa, S. S. (2017) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2017.04.028 · Cited by 40
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Wang, Y., Li, Y., He, C., Gou, B., & Song, M. (2018) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2018.12.008 · Cited by 44
Consequences of telomere shortening during lifespan
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“Identifying these rate-limiting tissues will provide targets on which to direct telomerase therapies thus correcting defects locally and possibly rescue whole body degeneration [45].”
BackgroundATP-Dependent Lon Protease Contributes to Helicobacter pylori-Induced Gastric Carcinogenesis
Luo, B., Wang, M., Hou, N., Hu, X., Jia, G., Qin, X., Zuo, X., Liu, Y., Luo, K., Song, W., et al. (2016) · Neoplasia · doi:10.1016/j.neo.2016.03.001 · Cited by 43
“Although severe mitochondrial dysfunction is detrimental, the salutary effects of mild mitochondrial perturbation have been reported in multiple organisms [17,36–38].”
BackgroundStress Signaling Between Organs in Metazoa
Owusu-Ansah, E., & Perrimon, N. (2015) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev-cellbio-100814-125523 · Cited by 39
“In addition, when mitochondrial function is impaired in the digestive tract by disruption of mitochondrial complex IV using an RNA interference (RNAi) construct targeting cytochrome c oxidase-1 subunit Vb (cco-1), the mitochondrial unfolded protein response (UPRmito) is induced in the intestine; surprisingly, UPRmito…”
MethodCross Talk of Proteostasis and Mitostasis in Cellular Homeodynamics, Ageing, and Disease
Gumeni, S., & Trougakos, I. P. (2016) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2016/4587691 · Cited by 43
Li, Q., Lu, H., Hu, G., Ye, Z., Zhai, D., Zhao, Y., Wang, L., An, X., & Lu, Z. (2019) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2019.03.194 · Cited by 43
Sural, S., Liang, C., Wang, F., Ching, T., & Hsu, A. (2020) · Science Advances · doi:10.1126/sciadv.aaz4452 · Cited by 39
“7 of 17 mitochondrial ETC components, isp-1 (complex III) and cco-1 (complex IV), are both dependent on the activity of UBL-5, a ubiquitin-like protein involved in UPRmt activation in worms (6, 37, 38).”
BackgroundInfluentialReduced insulin/IGF1 signaling prevents immune aging via ZIP-10/bZIP–mediated feedforward loop
Lee, Y., Jung, Y., Jeong, D., Hwang, W., Ham, S., Park, H. H., Kwon, S., Ashraf, J. M., Murphy, C. T., & Lee, S. (2021) · The Journal of Cell Biology · doi:10.1083/jcb.202006174 · Cited by 40
Sladowska, M., Turek, M., Kim, M., Drabikowski, K., Mussulini, B. H. M., Mohanraj, K., Serwa, R. A., Topf, U., & Chacińska, A. (2021) · PLoS Biology · doi:10.1371/journal.pbio.3001302 · Cited by 42
“UPRmt activation that is mediated by ATFS-1 has been implicated in life span extension upon impairments in genes that are associated with OXPHOS, mitochondrial chaperones and proteases, and the inhibition of mitochondrial translation [21,22,46].”
BackgroundSoo, S. K., Traa, A., Rudich, Z. D., Moldakozhayev, A., Mistry, M., & Raamsdonk, J. M. V. (2022) · Aging Cell · doi:10.1111/acel.13740 · Cited by 41
Morrow, G., Pécheur, M. L., & Tanguay, R. M. (2015) · Biogerontology · doi:10.1007/s10522-015-9591-y · Cited by 42
“Indeed, hsp22 is one of the most up-regulated genes in tko25 flies that have an insufficient mitochondrial translational capacity due to a mutation in mitoribosomal protein S12 (mRpS12) (Fernandez-Ayala et al. 2010).”
BackgroundInfluentialRauthan, M., Ranji, P., Abukar, R., & Pilon, M. (2015) · G3 Genes Genomes Genetics · doi:10.1534/g3.115.018598 · Cited by 39
“Is UPRmt activation sufficient to explain the lifespan extension of the nduf-7(et19) mutant, as has been suggested for other long-lived mutants (Durieux et al. 2011; Houtkooper et al. 2013)?”
BackgroundActivation of mitochondrial unfolded protein response protects against multiple exogenous stressors
Soo, S. K., Traa, A., Rudich, P. D., Mistry, M., & Raamsdonk, J. M. V. (2021) · Life Science Alliance · doi:10.26508/lsa.202101182 · Cited by 42
“Although a role for the mitoUPR in longevity has been reported (Durieux et al, 2011; Houtkooper et al, 2013; Berendzen et al, 2016; Merkwirth et al, 2016) and debated (Bennett et al, 2014; Bennett & Kaeberlein, 2014), little is known about the role of ATFS-1 in response to exogenous stressors.”
BackgroundMitochondrial chaperone TRAP1 activates the mitochondrial UPR and extends healthspan in Drosophila
Baqri, R. M., Pietron, A. V., Gokhale, R. H., Turner, B. A., Kaguni, L. S., Shingleton, A. W., Kunes, S. M., & Miller, K. E. (2014) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2014.09.002 · Cited by 39
“Modifying mitochondrial physiology in one tissue may influence function in others through cell non-autonomous stress response pathways (Durieux et al., 2011).”
BackgroundSuccinate Dehydrogenase Upregulation Destabilize Complex I and Limits the Lifespan of gas-1 Mutant
Pujol, C., Hench, I. B., Sumakovic, M., Hench, J., Mourier, A., Baumann, L. C., Pavlenko, V., & Trifunović, A. (2013) · PLoS ONE · doi:10.1371/journal.pone.0059493 · Cited by 40
“An upregulation of UPR was detected in nuo-6(qm200) (Figure S3), as previously demonstrated in other long-lived Mit mutants [30].”
BackgroundEditing activity for eliminating mischarged tRNAs is essential in mammalian mitochondria
Hilander, T., Zhou, X.-L., Konovalova, S. A., Zhang, F., Euro, L., Chilov, D., POUTANEN, M. H., Chihade, J. W., Wang, E., & Tyynismaa, H. (2017) · Nucleic Acids Research · doi:10.1093/nar/gkx1231 · Cited by 42
“Impaired mitochondrial protein quality control is associated with multiple pathologies, especially those affecting the central nervous system (9), and also contributes to organismal stress resistance and even longevity through induction of cellular stress responses such as the mitochondrial unfolded protein response (…”
BackgroundAutophagy-related proteins: Potential diagnostic and prognostic biomarkers of aging-related diseases
Miceli, C., Leri, M., Stefani, M., & Bucciantini, M. (2023) · Ageing Research Reviews · doi:10.1016/j.arr.2023.101967 · Cited by 39
Germain, D. (2016) · Advances in cancer research · doi:10.1016/bs.acr.2016.01.004 · Cited by 38
mtDNA, Metastasis, and the Mitochondrial Unfolded Protein Response (UPRmt)
Kenny, T. C., & Germain, D. (2017) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2017.00037 · Cited by 40
“elegans as a readout of the UPRmt and has formed an impressive body of literature that has expanded our understanding of the UPRmt in worms (Benedetti et al., 2006; Haynes et al., 2007, 2010; Durieux et al., 2011; Nargund et al., 2012; Mohrin et al., 2015; Merkwirth et al., 2016; Tian et al., 2016).”
BackgroundGenetic inhibition of an ATP synthase subunit extends lifespan in C. elegans
Xu, C., Hwang, W., Jeong, D., Ryu, Y., Ha, C. M., Lee, S., Liu, L., & He, Z. M. (2018) · Scientific Reports · doi:10.1038/s41598-018-32025-w · Cited by 36
Hijacking Cellular Stress Responses to Promote Lifespan
Dutta, N., Garcia, G., & Higuchi‐Sanabria, R. (2022) · Frontiers in Aging · doi:10.3389/fragi.2022.860404 · Cited by 35
Mitochondrial quality control pathways sense mitochondrial protein import
Lee-Glover, L. P., & Shutt, T. E. (2023) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2023.11.004 · Cited by 39
“Mitochondrial stress i n one cell or tissue can generate a “mitokine” signal that activates a stress response in other locations [58].”
BackgroundRole of Autophagy in the Control of Body Metabolism
Quan, W., & Lee, M. (2013) · Endocrinology and Metabolism · doi:10.3803/enm.2013.28.1.6 · Cited by 39
A Conserved Role for p48 Homologs in Protecting Dopaminergic Neurons from Oxidative Stress
Dib, P. B., Gnägi, B., Daly, F., Sabado, V., Tas, D., Glauser, D. A., Meister, P., & Nagoshi, E. (2014) · PLoS Genetics · doi:10.1371/journal.pgen.1004718 · Cited by 37
The Roles of Cellular and Organismal Aging in the Development of Late-Onset Maladies
Marques, F. C., Volovik, Y., & Cohen, E. (2014) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathol-012414-040508 · Cited by 38
Dialogue between E. coli free radical pathways and the mitochondria of C. elegans
Govindan, J. A., Jayamani, E., Zhang, X. L., Mylonakis, E. E., & Ruvkun, G. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1517448112 · Cited by 37
“elegans mitochondria-mediated longevity is cell-nonautonomous (42, 44).”
Herholz, M., Cores, E. C., Baumann, L. C., Kukat, A., Hermeling, J. C., Maciej, S., Szczepanowska, K., Pavlenko, V., Frommolt, P., & Trifunović, A. (2019) · Nature Communications · doi:10.1038/s41467-019-11275-w · Cited by 37
The intersection of exercise and aging on mitochondrial protein quality control
Zhang, Y., Oliveira, A. N., & Hood, D. A. (2020) · Experimental Gerontology · doi:10.1016/j.exger.2019.110824 · Cited by 40
Taylor, S. K. B., Minhas, M. H., Tong, J., Selvaganapathy, P. R., Mishra, R. K., & Gupta, B. P. (2021) · Scientific Reports · doi:10.1038/s41598-021-82466-z · Cited by 36
Mitochondrial Stress and Mitokines: Therapeutic Perspectives for the Treatment of Metabolic Diseases
Zhang, B., Chang, J. Y., Lee, M. H., Ju, S. H., Yi, H., & Shong, M. (2024) · Diabetes & Metabolism Journal · doi:10.4093/dmj.2023.0115 · Cited by 39
“This elusive signaling molecule is termed a “mitokine” [65], and its identity and mechanisms of action are not fully understood.”
BackgroundMitochondrial genetics, signalling and stress responses
Liu, Y. J., Sulc, J., & Auwerx, J. H. (2025) · Nature Cell Biology · doi:10.1038/s41556-025-01625-w · Cited by 38
“The study of mito–nuclear coordination and the MSR has received substantial interest since the discovery that MSR activation enhances longevity in model organisms 135,136,148 .”
Neuronal Inputs and Outputs of Aging and Longevity
Alcedo, J., Flatt, T., & PASYUKOVA, E. G. (2013) · Frontiers in Genetics · doi:10.3389/fgene.2013.00071 · Cited by 39
The Mitochondrial Unfolded Protein Response Protects against Anoxia in Caenorhabditis elegans
Peña, S., Sherman, T., Brookes, P. S., & Nehrke, K. W. (2016) · PLoS ONE · doi:10.1371/journal.pone.0159989 · Cited by 33
“Neuronal mitochondrial stress can be sensed remotely, suggesting that cells are able to coordinate adaptive responses based upon communicating the status of their mitochondria (Fig 3A) [14].”
Pyridine Dinucleotides from Molecules to Man
Fessel, J. P., & Oldham, W. M. (2017) · Antioxidants and Redox Signaling · doi:10.1089/ars.2017.7120 · Cited by 35
“Activation of the UPR promotes longevity in worms (51, 97).”
Mitochondrial disease, mitophagy, and cellular distress in methylmalonic acidemia
Luciani, A., Denley, M. C. S., Govers, L. P., Sorrentino, V., & Froese, D. S. (2021) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-021-03934-3 · Cited by 41
mtUPR Modulation as a Therapeutic Target for Primary and Secondary Mitochondrial Diseases
Cilleros-Holgado, P., Gómez-Fernández, D., Piñero-Pérez, R., Reche-López, D., Álvarez-Córdoba, M., Munuera-Cabeza, M., Talaverón-Rey, M., Povea-Cabello, S., Suárez-Carrillo, A., Romero-González, A., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24021482 · Cited by 38
“This was investigated using neuronal-specific mitochondrial stressors, which provoke intestinal and muscle mtUPR activation through the release of signaling factors [70,71].”
BackgroundWang, C., Yang, M., Liu, D., & Zheng, C. (2024) · Cell Reports · doi:10.1016/j.celrep.2024.113865 · Cited by 35
ANGPTL6 expression is coupled with mitochondrial OXPHOS function to regulate adipose FGF21
Kang, S., Yi, H., Choi, M. J., Ryu, M. J., Jung, S.-B., Chung, H. K., Chang, J. Y., Kim, Y. K., Lee, S. E., Kim, H. W., et al. (2017) · Journal of Endocrinology · doi:10.1530/joe-16-0549 · Cited by 36
Kim, B., Brandli, A. A., Mitrofanis, J., Stone, J., Purushothuman, S., & Johnstone, D. M. (2017) · Ageing Research Reviews · doi:10.1016/j.arr.2017.05.005 · Cited by 36
Role of Signaling Molecules in Mitochondrial Stress Response
Hill, S., Sataranatarajan, K., & Remmen, H. V. (2018) · Frontiers in Genetics · doi:10.3389/fgene.2018.00225 · Cited by 39
“showed that mitochondrial proteotoxic stress restricted to neuronal tissue induced the mitochondrial UPRMT in a heterologous tissue, the intestine (Durieux et al., 2011).”
Background‘Inside Out’– a dialogue between mitochondria and bacteria
Han, B., Lin, C.-C., Hu, G., & Wang, M. C. (2018) · FEBS Journal · doi:10.1111/febs.14692 · Cited by 37
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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