Evidence map›Paper›PMID 22282471›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2012

The nuclear receptor, Nor-1, markedly increases type II oxidative muscle fibers and resistance to fatigue.

Michael A Pearen, Natalie A Eriksson, Rebecca L Fitzsimmons, Joel M Goode, Nick Martel, Sofianos Andrikopoulos, George E O Muscat

Abstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. NOR-1 as a Context-Dependent Rheostat of Vascular and Cardiac Remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. NOR-1 Overexpression Elevates Myoglobin Expression via PERM1 and Enhances Mitochondrial Function and Endurance in Skeletal Muscles of Aged Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  9. Review
  10. Enhancement of physiology via adaptive transcription.Pflugers Archiv : European journal of physiology · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Exercise metabolism and adaptation in skeletal muscle.Nature reviews. Molecular cell biology · 2023
    Review
  18. Article
  19. Article
  20. Review
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

7 authors at 2 institutions in 1 country.

Michael A PearenInstitute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland 4072, Australia.
Natalie A Eriksson
Rebecca L Fitzsimmons
Joel M Goode
Nick Martel
Sofianos Andrikopoulos
George E O Muscat
University of Queensland · AUHeidelberg Repatriation Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear hormone receptors (NR) have been implicated as regulators of lipid and carbohydrate metabolism. The orphan NR4A subgroup has emerged as regulators of metabolic function. Targeted silencing of neuron-derived orphan receptor 1 (Nor-1)/NR4A3 in skeletal muscle cells suggested that this NR was necessary for oxidative metabolism in vitro. To investigate the in vivo role of Nor-1, we have developed a mouse model with preferential expression of activated Nor-1 in skeletal muscle. In skeletal muscle, this resulted in a marked increase in: 1) myoglobin expression, 2) mitochondrial DNA and density, 3) oxidative enzyme staining, and 4) genes/proteins encoding subunits of electron transport chain complexes. This was associated with significantly increased type IIA and IIX myosin heavy chain mRNA and proteins and decreased type IIB myosin heavy chain mRNA and protein. The contractile protein/fiber type remodeling driving the acquisition of the oxidative type II phenotype was associated with 1) the significantly increased expression of myocyte-specific enhancer factor 2C, and phospho-histone deacetylase 5, and 2) predominantly cytoplasmic HDAC5 staining in the Tg-Nor-1 mice. Moreover, the Nor-1 transgenic line displayed significant improvements in glucose tolerance, oxygen consumption, and running endurance (in the absence of increased insulin sensitivity), consistent with increased oxidative capacity of skeletal muscle. We conclude that skeletal muscle fiber type is not only regulated by exercise-sensitive calcineurin-induced signaling cascade but also by NR signaling pathways that operate at the nexus that coordinates muscle performance and metabolic capacity in this major mass tissue.

Indexed as

AnimalsBlood GlucoseGenes, MitochondrialHistone DeacetylasesHumansMaleMiceMice, Inbred C57BLMice, TransgenicMitochondriaMuscle Fibers, Fast-TwitchMyoglobinMyosin Heavy ChainsNADNuclear Receptor Subfamily 4, Group A, Member 3Oxidation-ReductionBlood GlucoseHdac5 protein, mouseHistone DeacetylasesMyoglobinMyosin Heavy ChainsNADNuclear Receptor Subfamily 4, Group A, Member 3Protein IsoformsSuccinate Dehydrogenase

Identifiers

PMID22282471
PMCPMC5417129
OpenAlexW1974855834

What OpenQuestion holds

Textmetadata
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.