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4-Octyl Itaconate Alleviates Myocardial Ischemia-Reperfusion Injury Through Promoting Angiogenesis via ERK Signaling Activation

ABSTRACT: 4-Octyl Itaconate Alleviates Myocardial Ischemia-Reperfusion Injury Through Promoting Angiogenesis via ERK Signaling Activation

PROVIDER: PRJNA1250479 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33133802_1.fastq.gz	Fastqsanger.gz
	SRR33133802_2.fastq.gz	Fastqsanger.gz
	SRR33133804_1.fastq.gz	Fastqsanger.gz
	SRR33133804_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

4-Octyl Itaconate Alleviates Myocardial Ischemia-Reperfusion Injury Through Promoting Angiogenesis via ERK Signaling Activation

Project description:Myocardial ischemia-reperfusion (IR) injury is a critical complication following revascularization therapy for ischemic heart disease. Itaconate, a macrophage-derived metabolite, has been implicated in inflammation and metabolic regulation. This study investigates the protective role of itaconate derivatives against IR injury. Using a mice model of IR injury, the impact of 7-day 4-Octyl itaconate (4-OI) administration on cardiac function is assessed. Exogenous administration of 4-OI significantly reduces myocardial damage, enhances angiogenesis, and alleviates myocardial hypoxia injury during reperfusion. RNA sequencing and molecular docking techniques are used to find the target of itaconate, and changes in cardiac function are observed in Immune-Responsive Gene1 (IRG1) global knockout mice. In cell culture studies, 4-OI promotes endothelial cell proliferation and migration, mediated by Mitogen-Activated Protein Kinases (MAPK) signaling pathway activation, particularly through Extracellular Signal-Regulated Kinase (ERK) signaling. Inhibition of ERK blocks these beneficial effects on endothelial cells. Furthermore, itaconate synthesis inhibition worsens myocardial damage, which is mitigated by 4-OI supplementation. The results indicate that 4-OI promotes angiogenesis by activating MAPK signaling via FMS-like tyrosine kinase 1 (Flt1), highlighting its potential as a therapeutic strategy for myocardial IR injury.

2025-04-15 | GSE294549 | GEO

4-Octyl Itaconate Alleviates Myocardial Ischemia-Reperfusion Injury Through Promoting Angiogenesis via ERK Signaling Activation.

| S-EPMC11904966 | biostudies-literature

RNA-seq Transcriptomic Analysis of 4-octyl itaconate Repressing Myogenic Differentiation

Project description:The 4-octyl itaconate O1_is a type of cell-permeable itaconate derivative. Studies have shown that with an anti-fibrotic effect in systemic sclerosis, the OI also affects osteoclast differentiation. The aim of this study was to explore the molecular mechanisms underlying the effects of OI on myoblast differentiation by RNA-seq analysis.

2023-10-10 | GSE213991 | GEO

Expression data from hiPSC derived WT and ISG15 KO endothelial cells stimulated with interferon-a and treated with itaconic acid, dimethyl itaconate, 4-octyl itaconate and ruxolitinib

Project description:Analysis of gene expression in WT and ISG15 KO endothelial cells, stimulated with IFNa and treated with Itaconic acid (IA), Dimethyl itaconate (DI), 4-octyl itaconate (4OI) and ruxolitinib (RUX) to investigate the effects of treatments on transcriptional response in the cells.

2022-06-07 | GSE168747 | GEO

10x single-cell RNAseq profiling of hiPSC derived WT and ISG15 KO macrophages stimulated with interferon-a and treated with itaconic acid, 4-octyl itaconate and ruxolitinib

Project description:WT and ISG15 KO macrophages were stimulated with interferon-a and treated with itaconic acid and 4-octyl itaconate as they are known for anti-inflammatory effects. In this experiment, we further explored how itaconic acid and 4-octyl itaconate can play its role keeping ruxolitinib as a positive control in order to inhibit JAK/STAT pathway

2022-06-07 | GSE168816 | GEO

Single-cell RNA sequencing analysis of the effect of 4-octyl itaconate administration on gene expression in immune cells isolated from traumatic brain injury mice brain

Project description:4-octyl itaconate regulates immune response of brain immune cells following traumatic brain injury.

2024-07-27 | GSE272808 | GEO

Effect of 4-octyl itaconate on gene expression of dendritic cells

Project description:Effect of 4-octyl itaconate on gene expression of dendritic cells

| PRJNA1117028 | ENA

RNA-seq Transcriptomic Analysis of 4-octyl itaconate Repressing Myogenic Differentiation

Project description:RNA-seq Transcriptomic Analysis of 4-octyl itaconate Repressing Myogenic Differentiation

| PRJNA883422 | ENA

Expression data from PBMCs infected with influenza A virus and treated with/without Itaconate

Project description:Analysis of gene expression in human PBMCs infected with influenza A virus or Mock and treated with Itaconic acid, Dimethyl itaconate or 4-Octyl itaconate to investigate the effects itaconate have on transcriptional response in human PBMCs. We particularly looked at anti-inflammatory effects of itaconate in inflammation followed by Influenza A virus infection.

2021-10-31 | GSE162210 | GEO

Endogenous itaconate is not required for particulate matter-induced NRF2 expression or inflammatory response

Project description:RNA-sequencing demonstrated Acod1 (Aconitate decarboxylase 1) as one of the top genes induced by air polution particulate matter (PM) in macrophages. We therefore sought to determine the effect of both exogenous itaconate (4-octyl itaconate) and endogenous itaconate on PM-induced inflammation in macrophages through RNA sequencing.

2020-04-07 | GSE143881 | GEO

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