Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

OGT-mediated O-GlcNAcylation regulates macrophage polarization in heart failure via targeting IRF1.

BMC cardiovascular disorders - 30 Dec 2024

Jing Guoqiang, Ma Yuhong

Abstract excerpt

BACKGROUND: Heart failure (HF) is a syndrome with complex etiology and high mortality in the world. Macrophage-related inflammation is involved in HF development. O-GlcNAcylation is a post-translational modification that affects pathological processes. This study aimed to investigate the role of O-GlcNAcylation in HF, especially its effect on macrophage polarization. METHODS: Raw264.7 cells were treated with...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Acylation
Share to Fibrosis
Share to Heart Failure

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Interferon Regulatory Factor-1

Share to Lipopolysaccharides

Share to Macrophage Activation

Share to N-Acetylglucosaminyltransferases

Share to RAW 264.7 Cells

Source

Open in PubMed Open full text

Identifiers

PMID: 39736588
DOI: 10.1186/s12872-024-04429-2
PMCID: PMC11684060

Genes

OGT

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

OGT-mediated O-GlcNAcylation regulates macrophage polarization in heart failure via targeting IRF1.PMID 39736588Read ↗

Excessive <i>O</i> - GlcNAcylation causes heart failure and sudden deathSemantic proximity Read ↗

Macrophage Histone Lactylation Drives Inflammatory Activation in Heart Failure via the IFIT3/JNK Signaling AxisSemantic proximity Read ↗

LPS induces GFAT2 expression to promote O-GlcNAcylation and attenuate inflammation in macrophagesSemantic proximity Read ↗

Sirtuins regulate macrophage polarization in heart failure: Metabolic reprogramming, epigenetic regulation, and immune cell interactionsSemantic proximity Read ↗

FTO O-GlcNAcylation downregulates NLRP3 inflammasome and pyroptosis in macrophagesSemantic proximity Read ↗

IFIT3 Knockdown Attenuates Pressure-Overload-Induced Cardiac Inflammation and Remodeling Through a JNK/H3K9 Lactylation-Associated MechanismSemantic proximity Read ↗

The role of post‐translational modifications in cardiac hypertrophySemantic proximity Read ↗

A Transient Increase in Cardiomyocyte Protein O-GlcNAcylation Enhances Susceptibility to Pressure Overload-Induced Cardiac RemodelingSemantic proximity Read ↗

The Role of Inflammasomes in Heart FailureSemantic proximity Read ↗

Multimarker profiling identifies protective and harmful immune processes in heart failure: findings from BIOSTAT-CHFSemantic proximity Read ↗

ZDHHC14-Mediated Palmitoylation of TBK1 Promotes Pathological Cardiac Hypertrophy via Type I Interferon Signaling ActivationSemantic proximity Read ↗

The Essential Role of FoxO1 in the Regulation of Macrophage FunctionSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.