Evidence map›Paper›PMID 35327619›Full record

ReviewBiomolecules2022

Nuclear-Mitochondrial Interactions.

Brittni R Walker, Carlos T Moraes

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
8.6field-weighted citation impact, top 1% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

  1. Modelling mitochondrial diseases in neuronsJournal of neuromuscular diseases · 2025
    Pooled it
  2. Trial
  3. Article
  4. Mitochondrial dysfunction in urologic disease.Prostate cancer and prostatic diseases · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Mitochondrial complex I deficiency-associated diseases and models.Cellular and molecular life sciences : CMLS · 2026
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

14 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Brittni R WalkerNeuroscience Program, University of Miami Miller School of Medicine, 1420 NW 9th Avenue, Rm. 229, Miami, FL 33136, USA.
Carlos T MoraesDepartment of Neurology, University of Miami Miller School of Medicine, 1420 NW 9th Avenue, Rm. 229, Miami, FL 33136, USA.ORCID 0000-0002-8077-7092
University of Miami · US

Funding

SETTING THE STAGE FOR REPLACEMENT OF MITOCHONDRIAL GENESR01EY010804 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 1995 to 2025
$9.4M
Cellular and Molecular Consequences of Respiratory Chain Defects in NeuronsR01NS079965 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 2012 to 2023
$3.9M
Imaging mitochondrial signaling in B-cells ectopically implanted in the eyeR33ES025673 · NIEHS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI CAICEDO, ALEJANDRO, MORAES, CARLOS TORRES · 2018 to 2019
$761k
NEI NIH HHS R01 EY010804NIEHS NIH HHS R33 ES025673NINDS NIH HHS R01 NS079965
6 · The paper itself

Abstract

Mitochondria, the cell's major energy producers, also act as signaling hubs, interacting with other organelles both directly and indirectly. Despite having its own circular genome, the majority of mitochondrial proteins are encoded by nuclear DNA. To respond to changes in cell physiology, the mitochondria must send signals to the nucleus, which can, in turn, upregulate gene expression to alter metabolism or initiate a stress response. This is known as retrograde signaling. A variety of stimuli and pathways fall under the retrograde signaling umbrella. Mitochondrial dysfunction has already been shown to have severe implications for human health. Disruption of retrograde signaling, whether directly associated with mitochondrial dysfunction or cellular environmental changes, may also contribute to pathological deficits. In this review, we discuss known signaling pathways between the mitochondria and the nucleus, examine the possibility of direct contacts, and identify pathological consequences of an altered relationship.

Indexed as

Cell NucleusMitochondriaHumansMitochondrial ProteinsSignal TransductionMitochondrial Proteinsintegrated stress responseMAMsmitochondrianucleusretrograde signaling

Identifiers

PMID35327619
PMCPMC8946195
OpenAlexW4220918420

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.