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Paper · 41220146

Nuclear Receptor Subfamily 4 Group A Member 1 Exacerbates Cardiac Remodeling by Inhibiting Mitochondrial Function Through the Peroxisome Proliferator-Activated Receptor γ Coactivator-1α/Nuclear Respiratory Factor 1/Transcription Factor A Mitochondrial Axis.

Kong CY and 5 others. J Am Heart Assoc, 2025. Cited by 0 papers, by iCite.

11 sourcespapers-2026-11-12-0.1.0

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ConductScience Library. Nuclear Receptor Subfamily 4 Group A Member 1 Exacerbates Cardiac Remodeling by Inhibiting Mitochondrial Function Through the Peroxisome Proliferator-Activated Receptor γ Coactivator-1α/Nuclear Respiratory Factor 1/Transcription Factor A Mitochondrial Axis. Papers, record 41220146. Release papers-2026-11-12-0.1.0, 12 Nov 2026. https://conductscience.org/library/papers/41220146

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Paper

PubMed's record of the paper, with iCite's citation figures. No abstract is shown.

Title
Nuclear Receptor Subfamily 4 Group A Member 1 Exacerbates Cardiac Remodeling by Inhibiting Mitochondrial Function Through the Peroxisome Proliferator-Activated Receptor γ Coactivator-1α/Nuclear Respiratory Factor 1/Transcription Factor A Mitochondrial Axis.
PubMed
Journal
J Am Heart Assoc
PubMed
Year
2025
PubMed
Publication types
Journal Article, Research Support, Non-U.S. Gov't
PubMed
Citations, by iCite
0
iCite
Revised in PubMed
2026-09-02
PubMed

Authors6

The authors in the order PubMed's record lists them, with the ORCID iDs it states.

OrderAuthorForenameKindORCID iD
1Kong CYChun-Yan
2Wang MYMing-Yu
3Ma YLYu-Lanhttps://orcid.org/0009-0008-9451-6230
4Guo ZZhen
5Yang ZZheng
6Tang QZQi-Zhuhttps://orcid.org/0000-0003-2210-3169

Source PubMed

Topics19

NLM's MeSH indexing of the paper, its major topics first.

MeSH termMajor
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMajor topic
Ventricular RemodelingMajor topic
Nuclear Receptor Subfamily 4, Group A, Member 1Major topic
Mitochondria, HeartMajor topic
Myocytes, CardiacMajor topic
Nuclear Respiratory Factor 1Major topic
CardiomegalyMajor topic
Transcription FactorsMajor topic
Animals
Rats
Disease Models, Animal
Mice, Knockout
Mice
Male
Mice, Inbred C57BL
Signal Transduction
Rats, Sprague-Dawley
Heart Failure
Cells, Cultured

Source PubMed

Grants0

Each grant PubMed's record writes, matched to the NIH project NIH's grant and paper links name for this paper, and each of those links the record does not write.

None in this release.

Trials0

The trials whose ClinicalTrials.gov record lists the paper, and the trial numbers the paper's PubMed record names.

None in this release.

Comments and corrections0

PubMed's comments and corrections, NLM's own indexing: retractions first, then expressions of concern, errata and updates, and comments last.

None in this release.

References45

The papers the reference list in PubMed's record names, those in our copy of PubMed, in the list's order.

OrderPMIDTitleJournalYearIn PapersSource
133,087,562Blocking PPARγ interaction facilitates Nur77 interdiction of fatty acid uptake and suppresses breast cancer progression.Proc Natl Acad Sci U S A2020https://conductscience.org/library/papers/33087562PubMed
228,004,807Expert consensus document: Mitochondrial function as a therapeutic target in heart failure.Nat Rev Cardiol2017https://conductscience.org/library/papers/28004807PubMed
338,834,564Semaglutide ameliorates cardiac remodeling in male mice by optimizing energy substrate utilization through the Creb5/NR4a1 axis.Nat Commun2024https://conductscience.org/library/papers/38834564PubMed
438,422,699Nur77 increases mitophagy and decreases aggregation of α-synuclein by modulating the p-c-Abl/p-PHB2 Y121 in α-synuclein PFF SH-SY5Y cells and mice.Eur J Med Chem2024https://conductscience.org/library/papers/38422699PubMed
531,462,501Inhibition of NR4A1 Promotes ROS Accumulation and IL24-Dependent Growth Arrest in Rhabdomyosarcoma.Mol Cancer Res2019https://conductscience.org/library/papers/31462501PubMed
630,827,145HIMF (Hypoxia-Induced Mitogenic Factor)-IL (Interleukin)-6 Signaling Mediates Cardiomyocyte-Fibroblast Crosstalk to Promote Cardiac Hypertrophy and Fibrosis.Hypertension2019https://conductscience.org/library/papers/30827145PubMed
735,577,178Kallistatin/Serpina3c inhibits cardiac fibrosis after myocardial infarction by regulating glycolysis via Nr4a1 activation.Biochim Biophys Acta Mol Basis Dis2022https://conductscience.org/library/papers/35577178PubMed
838,794,753Fucoidan Improves D-Galactose-Induced Cognitive Dysfunction by Promoting Mitochondrial Biogenesis and Maintaining Gut Microbiome Homeostasis.Nutrients2024https://conductscience.org/library/papers/38794753PubMed
937,994,595USP28 Serves as a Key Suppressor of Mitochondrial Morphofunctional Defects and Cardiac Dysfunction in the Diabetic Heart.Circulation2024https://conductscience.org/library/papers/37994595PubMed
1033,762,571FGF1ΔHBS prevents diabetic cardiomyopathy by maintaining mitochondrial homeostasis and reducing oxidative stress via AMPK/Nur77 suppression.Signal Transduct Target Ther2021https://conductscience.org/library/papers/33762571PubMed

Cited by0

The papers in our copy of PubMed whose reference list names this one, newest first. iCite, which reads more sources, counts 0 citations.

None in this release.

Genes0

The genes the Gene search release ties to the paper: Swiss-Prot's references first, then PubTator's text mining.

None in this release.

Drugs0

The drugs whose trials, in the Pipelines release, list the paper.

None in this release.

Data0

The data bank entries PubMed's record names. Trial numbers are under Trials.

None in this release.

Data dates

The date of each source this release read.

PubMed
2026-11-06
PubMed
iCite
2026-11-05
iCite
PMC's ID file
2026-11-05
PMC's ID file
NIH RePORTER's grant and paper links
2026-11-01
NIH RePORTER's grant and paper links
Trials
2026-11-12
Gene search
2026-11-11
Pipelines
2026-09-18

Sources 11

  • ChEMBL, through Open TargetsCC BY-SA 3.0
  • ClinicalTrials.govNo license stated
  • HGNCCC0
  • iCiteCC BY 4.0
  • NCBI GenePublic domain (US government)
  • NIH RePORTER's grant and paper linksPublic domain
  • Open TargetsCC0 1.0
  • PMC's ID filePublic domain (US government)
  • PubMedNLM's terms
  • PubTator 3Public domain
  • UniProtCC BY 4.0
Each source's terms
  • ChEMBL, through Open TargetsCC BY-SA 3.0, for the parts from ChEMBL. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
  • ClinicalTrials.govnone stated
  • HGNCCC0: https://www.genenames.org/about/license/
  • iCiteCC BY 4.0
  • NCBI GeneNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
  • NIH RePORTER's grant and paper linksPublic domain (NIH RePORTER)
  • Open TargetsCC0 1.0. Open Targets asks that users cite its latest paper: Buniello et al. 2025, Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery, Nucleic Acids Research 53(D1):D1467, PMID 39657122. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
  • PMC's ID fileNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
  • PubMedNLM's terms
  • PubTator 3Public domain
  • UniProtCC BY 4.0. UniProt's licence file: "All databases and documents in the UniProt FTP directory may be copied and redistributed freely, without advance permission, provided that this copyright statement is reproduced with each copy." UniProt asks that users cite its latest paper: The UniProt Consortium, UniProt: the Universal Protein Knowledgebase in 2025, Nucleic Acids Research 53:D609-D617, https://doi.org/10.1093/nar/gkae1010. Read on 9 Nov 2026 at https://www.uniprot.org/help/license

ClinicalTrials.gov's data carry an international copyright outside the United States: https://clinicaltrials.gov/about-site/terms-conditions.

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