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Mitochondrial-to-nuclear communication in aging: an epigenetic perspective

Journal

TRENDS IN BIOCHEMICAL SCIENCES
Volume 47, Issue 8, Pages 645-659

Publisher

CELL PRESS
DOI: 10.1016/j.tibs.2022.03.008

Keywords

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Funding

  1. National Key R&D Program of China [2017YFA0506400]
  2. Strategic Priority Research Program of the Chinese Academy of Sciences [XDB39000000]
  3. National Natural Science Foundation of China [31930023]

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Mitochondrial changes associated with aging play a crucial role in the aging process by modulating epigenomes through communication with the nucleus.
Age-associated changes in mitochondria are closely involved in aging. Apart from the established roles in bioenergetics and biosynthesis, mitochondria are signaling organelles that communicate their fitness to the nucleus, triggering transcriptional programs to adapt homeostasis stress that is essential for organismal health and aging. Emerging studies revealed that mitochondrial-to-nuclear (mito-nuclear) communication via altered levels of mitochondrial metabolites or stress signals causes various epigenetic changes, facilitating efforts to maintain homeostasis and affect aging. Here, we summarize recent studies on the mechanisms by which mito-nuclear communication modulates epigenomes and their effects on regulating the aging process. Insights into understanding how mitochondrial metabolites serve as prolongevity signals and how aging affects this communication will help us develop interventions to promote longevity and health.

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