Cited by 15Genetics, Aging, and Longevity in Model OrganismsMitochondrial Function and PathologyAutophagy in Disease and Therapy

Collaboration between mitochondria and the nucleus is key to long life in Caenorhabditis elegans

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Chang, Hsin-Wen, Shtessel, Ludmila, Lee, Siu Sylvia·2015·Free Radical Biology and Medicine

Abstract

Recent findings in diverse organisms strongly support a conserved role for mitochondrial electron transport chain dysfunction in longevity modulation, but the underlying mechanisms are not well understood. One way cells cope with mitochondrial dysfunction is through a retrograde transcriptional reprogramming response. In this review, we primarily focus on the work that has been performed in Caenorhabditis elegans to elucidate these mechanisms. We describe several transcription factors that participate in mitochondria-to-nucleus signaling and discuss how they mediate the relationship between mitochondrial dysfunction and life span.

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Crossref · 10.1016/j.freeradbiomed.2014.10.576

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  • In worms, lifespan extension from electron transport chain component knockdown depends on a mitochondria-responsive transcription program including NRF2/SKN-1 and p53/CEP-1.

    “In worms, lifespan extension through knockdown of an electron transport chain component is dependent on a complex mitochondria-responsive transcription regulatory program that includes the ROS-sensitive transcription factors NRF2/SKN-1 and p53/CEP-1 (Chang et al., 2015).”

    From The Aging Epigenome (2016) · cites this paper as Chang et al., 2015

  • Nuclear-mitochondrial communication is a key determinant of longevity in animals.

    “nuclear-mitochondrial communication is also a key determinant of longevity in animals (Chang et al., 2015; Gomes et al., 2013).”

    From The Aging Epigenome (2016) · cites this paper as Chang et al., 2015

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References 122 · Cited by 15

Research works printed but not linked: 2

  1. [48]Hwang AB Ryu E Artan M Chang H Humayun M Nam H Feedback regulation via AMPK and HIF-1 mediates ROS-dependent longevity in Caenorhabditis elegans PMC4210294 25288734
  2. [98]Hagopian K Harper M-E Ram JJ Humble SJ Weindruch R Ramsey JJ Long-term calorie restriction reduces proton leak and hydrogen peroxide production in liver mitochondria Am J Physiol Endocrinol Metab 288 E674 84 2005 15562252

Authors
Chang, H.-W., Shtessel, L., & Lee, S. S.
Affiliations
Cornell University (US)
Venue
Free Radical Biology and Medicine
Publisher
Elsevier BV
Published
2015-01
Volume
78
Pages
168-178
ISSN
0891-5849 (ISSN-L)
OpenAlex
W2062385079
Cited by
15
References
122
Citations by year
2023: 1 · 2022: 1 · 2021: 2 · 2020: 1 · 2018: 2 · 2017: 1 · 2016: 5 · 2015: 2
FWCI
0.30
Type
journal article
Language
en
Open access
Locations
  • Free Radical Biology and Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute on Aging (R01AG024425)
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
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
mitochondrial dysfunction, electron transport chain, longevity, lifespan, retrograde signaling, transcription factors, Caenorhabditis elegans, aging
MeSH terms
Animals, Cell Nucleus, Longevity, Mitochondria, Transcription Factors, Signal Transduction, Caenorhabditis elegans, Caenorhabditis elegans Proteins

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