Evidence map›Paper›PMID 20533901›Full record

ReviewEssays in biochemistry2010

Regulation of mitochondrial biogenesis.

François R Jornayvaz, Gerald I Shulman

Abstract readReview
In one paragraph

Review in Essays in biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 581 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
581citing papers in PubMed, 2 pooled it
4.5field-weighted citation impact, top 5% 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

581 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,115 citations in OpenAlex.

  1. Effects of selected dietary supplements on migraine prophylaxis: A systematic review and dose-response meta-analysis of randomized controlled trials.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Pooled it
  2. Association between theFrontiers in physiology · 2025
    Pooled it
  3. Review
  4. Review
  5. Article
  6. Review
  7. Renal gluconeogenesis: a key metabolic hub in health and kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

521 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 2 institutions in 1 country.

François R JornayvazDepartment of Internal Medicine, Yale University School of Medicine, New Haven, CT 06536, USA.
Gerald I Shulman
Howard Hughes Medical Institute · USYale University · US

Funding

Yale Mouse Metabolic Phenotyping CenterU24DK059635 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 2001 to 2015
$8.9M
Mechanisms of Lipid-Induced Hepatic Insulin ResistanceR01DK040936 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 1989 to 2015
$5.1M
Howard Hughes Medical InstituteNIDDK NIH HHS R01 DK040936NIDDK NIH HHS U24 DK059635
6 · The paper itself

Abstract

Although it is well established that physical activity increases mitochondrial content in muscle, the molecular mechanisms underlying this process have only recently been elucidated. Mitochondrial dysfunction is an important component of different diseases associated with aging, such as Type 2 diabetes and Alzheimer's disease. PGC-1alpha (peroxisome-proliferator-activated receptor gamma co-activator-1alpha) is a co-transcriptional regulation factor that induces mitochondrial biogenesis by activating different transcription factors, including nuclear respiratory factor 1 and nuclear respiratory factor 2, which activate mitochondrial transcription factor A. The latter drives transcription and replication of mitochondrial DNA. PGC-1alpha itself is regulated by several different key factors involved in mitochondrial biogenesis, which will be reviewed in this chapter. Of those, AMPK (AMP-activated protein kinase) is of major importance. AMPK acts as an energy sensor of the cell and works as a key regulator of mitochondrial biogenesis. AMPK activity has been shown to decrease with age, which may contribute to decreased mitochondrial biogenesis and function with aging. Given the potentially important role of mitochondrial dysfunction in the pathogenesis of numerous diseases and in the process of aging, understanding the molecular mechanisms regulating mitochondrial biogenesis and function may provide potentially important novel therapeutic targets.

Indexed as

AMP-Activated Protein KinasesDNA, MitochondrialMitochondriaModels, BiologicalOrganelle BiogenesisAMP-Activated Protein KinasesDNA, Mitochondrial

Identifiers

PMID20533901
PMCPMC3883043
OpenAlexW2110374590

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.