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REDD1 Deletion Suppresses NF-κB Signaling in Cardiomyocytes and Prevents Deficits in Cardiac Function in Diabetic Mice

International Journal of Molecular Sciences(2024)10.3390/ijms25126461Source: DataRank Database

REDD1 Deletion Suppresses NF-κB Signaling in Cardiomyocytes and Prevents Deficits in Cardiac Function in Diabetic Mice is a research paper published in International Journal of Molecular Sciences (2024). On theSindex it has a DataRank of 0. It has been cited 6 times.

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Open Access6 citations

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›Methodology & internals

datarank_citation_only_1hop_v6· scope data_onlyMethodology

Pipeline:MetadataData-paper checkEnrichmentCitation networkScoring

Enrichment:Funding (10 grants)Impact (FWCI 1.09)OA: goldTopics (82)IDs (PubMed, OpenAlex)SDGs (1)

FAIR Checklist

Context only (not used in score)

Findable (1/2)

Has DOI

Accessible (1/2)

Open Access

Interoperable (0/2)

Reusable (0/3)

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Authors (8)

Siddharth Sunilkumar ORCID,Sandeep Subrahmanian ORCID,Allyson L. Toro,Omer Cavus ORCID,Efosa V. Omorogbe

Live enrichment

PubMed:38928166 OpenAlex:https://openalex.org/W4399583409

National Institutes of Health

Grant: F31 HL165924

National Institutes of Health

Grant: R01 EY029702

National Institutes of Health

Grant: 1-INO-2024-1538-A-N

National Institutes of Health

Grant: 11-23-PDF-84

National Institutes of Health

Grant: 898925

NIH HHS

Grant: 1F31HL165924-01A1

NEI NIH HHS

Grant: R01 EY032879

NIH HHS

Grant: 1R01EY029702-04A1

National Institutes of Health

Grant: 3R01EY029702-02S1

Targeting the Etiology of Diabetic Retinopathy

National Institutes of Health

Grant: 5F31HL165924-03

Role of Diabetes-Induced REDD1 in Heart Disease

FWCI

1.09

Citation Percentile

0.8%

Citation Trend

2024

2025

2026

goldLicense: cc-by

journalhttps://www.mdpi.com/1422-0067/25/12/6461/pdf?version=1718262616

publisherhttps://www.mdpi.com/1422-0067/25/12/6461/pdf?version=1718262616

publisherhttps://www.mdpi.com/1422-0067/25/12/6461/pdf

journalhttps://doi.org/10.3390/ijms25126461

repositoryhttps://pubmed.ncbi.nlm.nih.gov/38928166

Fields of Study

NF-κB Signaling PathwaysSignaling Pathways in DiseasePeroxisome Proliferator-Activated Receptors0301 basic medicine03 medical and health sciences0303 health sciencesAnimalsMyocytes, CardiacNF-kappa BSignal TransductionMiceDiabetes Mellitus, ExperimentalTranscription FactorsGlycogen Synthase Kinase 3 betaHumansMice, KnockoutMaleChemokine CCL2Interleukin-1betaMice, Inbred C57BLTumor Necrosis Factor-alphaPhosphorylationGene Deletion

MeSH Terms

Glycogen Synthase Kinase 3 betaAnimalsDiabetes Mellitus, ExperimentalHumansMaleMice, Inbred C57BLPhosphorylationTranscription FactorsTumor Necrosis Factor-alphaSignal TransductionNF-kappa BGene DeletionMice, KnockoutChemokine CCL2Myocytes, CardiacMiceInterleukin-1beta

Keywords

Transcription factorEndocrinologyNF-κBInternal medicineDownregulation and upregulationProinflammatory cytokineDiabetic cardiomyopathyDiabetes mellitusChemokineCardiac function curveCytokineSignal transductionInflammationNFKB1Ejection fractionBiologyMedicineCell biologyHeart failureGeneCardiomyopathyBiochemistryHeart DiseaseRtp801Ddit4MaleInterleukin-1betaArticleDiabetes Mellitus, ExperimentalMiceAnimalsHumansMyocytes, CardiacPhosphorylationChemokine CCL2Mice, KnockoutGlycogen Synthase Kinase 3 betaTumor Necrosis Factor-alphaNF-kappa BMice, Inbred C57BLGene DeletionTranscription Factors

Sustainable Development Goals

SDG 0: Good health and well-being