Evidence map›Paper›PMID 32001259›Full record

ReviewRedox biology2020

Estrogenic control of mitochondrial function.

Carolyn M Klinge

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
193citing papers in PubMed, 1 pooled it
10.6field-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

193 citing papers in PubMed, 1 synthesis or guideline pooled it, 263 citations in OpenAlex.

  1. The Role of Estrogen in Mitochondrial Disease.Cellular and molecular neurobiology · 2025
    Pooled it
  2. Trial
  3. Review
  4. Review
  5. Review
  6. Article
  7. HSP90α lactylation orchestrates PGC1α and LRPGC1 nuclear translocation driving mitochondrial biogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  8. Review
  9. Endocrine Disruptors and Gynecological Malignancies.Diagnostics (Basel, Switzerland) · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Sex determines cardiac and renal Vulnerability to chronic hemoglobin toxicity.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026
    Article
  17. Review
  18. Article
  19. Review
  20. Article

133 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

1 author at 1 institution in 1 country.

Carolyn M KlingeDepartment of Biochemistry and Molecular Genetics, University of Louisville School of Medicine, Louisville, 40292, KY, USA. Electronic address: carolyn.klinge@louisville.edu.
University of Louisville · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sex-based differences in human disease are caused in part by the levels of endogenous sex steroid hormones which regulate mitochondrial metabolism. This review updates a previous review on how estrogens regulate metabolism and mitochondrial function that was published in 2017. Estrogens are produced by ovaries and adrenals, and in lesser amounts by adipose, breast stromal, and brain tissues. At the cellular level, the mechanisms by which estrogens regulate diverse cellular functions including reproduction and behavior is by binding to estrogen receptors α, β (ERα and ERβ) and G-protein coupled ER (GPER1). ERα and ERβ are transcription factors that bind genomic and mitochondrial DNA to regulate gene transcription. A small proportion of ERα and ERβ interact with plasma membrane-associated signaling proteins to activate intracellular signaling cascades that ultimately alter transcriptional responses, including mitochondrial morphology and function. Although the mechanisms and targets by which estrogens act directly and indirectly to regulate mitochondrial function are not fully elucidated, it is clear that estradiol regulates mitochondrial metabolism and morphology via nuclear and mitochondrial-mediated events, including stimulation of nuclear respiratory factor-1 (NRF-1) transcription that will be reviewed here. NRF-1 is a transcription factor that interacts with coactivators including peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (PGC-1α) to regulate nuclear-encoded mitochondrial genes. One NRF-1 target is TFAM that binds mtDNA to regulate its transcription. Nuclear-encoded miRNA and lncRNA regulate mtDNA-encoded and nuclear-encoded transcripts that regulate mitochondrial function, thus acting as anterograde signals. Other estrogen-regulated mitochondrial activities including bioenergetics, oxygen consumption rate (OCR), and extracellular acidification (ECAR), are reviewed.

Indexed as

MitochondriaTranscription FactorsDNA, MitochondrialEstrogensHumansNuclear Respiratory Factor 1DNA, MitochondrialEstrogensNuclear Respiratory Factor 1Transcription FactorsEstrogenEstrogen receptorGPER1MitochondriaNRF-1Sex-differences

Identifiers

PMID32001259
PMCPMC7212490
OpenAlexW3002156037

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.