Evidence map›Paper›PMID 31997134›Full record

ReviewHuman genetics2020

Mitonuclear genomics and aging.

Joseph C Reynolds, Conscience P Bwiza, Changhan Lee

Open access · greenAbstract readReview
In one paragraph

Review in Human genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Mitochondrial signal transduction.Cell metabolism · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Characterization of whole mitogenome sequence of the Tongde yak (Mitochondrial DNA. Part B, Resources · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 2 countries.

Joseph C ReynoldsLeonard Davis School of Gerontology, University of Southern California, Los Angeles, CA, 90089, USA.
Conscience P BwizaLeonard Davis School of Gerontology, University of Southern California, Los Angeles, CA, 90089, USA.
Changhan LeeLeonard Davis School of Gerontology, University of Southern California, Los Angeles, CA, 90089, USA. changhan.lee@usc.edu.ORCID http://orcid.org/0000-0003-0327-4712
University of Southern California · US

Funding

USC Geroscience Training in the Biology of AgingT32AG052374 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Sean P CURRAN · 2016 to 2026
$5.3M
Use of viral-vectors for studying effects of chronic inflammation on executive functionR01AG052258 · NIA · UNIVERSITY OF FLORIDA · PI FOSTER, THOMAS C · 2016 to 2020
$1.9M
Novel Regulators of Aging Metabolism Encoded in the Mitochondrial GenomeR01AG052558 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LEE, CHANGHAN · 2016 to 2020
$1.8M
American Association of University Women FellowshipNIA NIH HHS AG052558NIA NIH HHS R01 AG052258NIA NIH HHS R01 AG052558NIA NIH HHS T32 AG052374NIA NIH HHS T32 training grantUniversity of Southern California Endowed fellowship
6 · The paper itself

Abstract

Our cells operate based on two distinct genomes that are enclosed in the nucleus and mitochondria. The mitochondrial genome presumably originates from endosymbiotic bacteria. With time, a large portion of the original genes in the bacterial genome is considered to have been lost or transferred to the nuclear genome, leaving a reduced 16.5 Kb circular mitochondrial DNA (mtDNA). Traditionally only 37 genes, including 13 proteins, were thought to be encoded within mtDNA, its genetic repertoire is expanding with the identification of mitochondrial-derived peptides (MDPs). The biology of aging has been largely unveiled to be regulated by genes that are encoded in the nuclear genome, whereas the mitochondrial genome remained more cryptic. However, recent studies position mitochondria and mtDNA as an important counterpart to the nuclear genome, whereby the two organelles constantly regulate each other. Thus, the genomic network that regulates lifespan and/or healthspan is likely constituted by two unique, yet co-evolved, genomes. Here, we will discuss aspects of mitochondrial biology, especially mitochondrial communication that may add substantial momentum to aging research by accounting for both mitonuclear genomes to more comprehensively and inclusively map the genetic and molecular networks that govern aging and age-related diseases.

Indexed as

AgingAnimalsCell NucleusDNA, MitochondrialGenome, MitochondrialGenomicsHumansLongevityMitochondriaDNA, Mitochondrial

Identifiers

PMID31997134
PMCPMC7147958
OpenAlexW3003915262

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.