Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Resveratrol Suppresses Susceptibility of Ventricular Arrhythmia in Heart Failure Model

ABSTRACT: In a rabbit heart failure model, resveratrol treatment restored cardiac function, normalized calcium handling, and reduced ventricular arrhythmia by reversing ion channel downregulation, fibrosis, apoptosis, and inflammation. These findings highlight resveratrol’s cardioprotective potential as a therapeutic strategy against arrhythmia in heart failure.

INSTRUMENT(S):

ORGANISM(S): Oryctolagus Cuniculus (rabbit)

TISSUE(S): Heart

SUBMITTER: Chen-Chung Liao

LAB HEAD: Chen-Chung Liao

PROVIDER: PXD069110 | Pride | 2026-01-12

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20241008-micropac110cm-DIA120min-C20240001_N6.raw	Raw
	20241008-micropac110cm-DIA120min-C20240002_N9.raw	Raw
	20241008-micropac110cm-DIA120min-C20240003_N10.raw	Raw
	20241008-micropac110cm-DIA120min-C20240004_HF311.raw	Raw
	20241008-micropac110cm-DIA120min-C20240005_HF327.raw	Raw

Items per page:

1 - 5 of 11

Publications

Resveratrol suppresses susceptibility of ventricular arrhythmia in heart failure model.

Tsai Yung-Nan YN Hsiao Ya-Wen YW Chang Ting-Yung TY Liao Chen-Chung CC Lin Chin-Yu CY Hsieh Yu-Cheng YC Chao Tze-Fan TF Li Guan-Yi GY Huang Yu-Ting YT Higa Satoshi S Chen Shih-Ann SA Chang Shih-Lin SL

BMC cardiovascular disorders 20251204 1

PMID: 41345537

Similar Datasets

Effect of resveratrol on avian pathogenic Escherichia coli

Project description:APEC cells treated by resveratrol were investigated using a label-free differential proteomics method.

2021-11-03 | PXD025706 | Pride

Resveratrol suppresses susceptibility of ventricular arrhythmia in heart failure model.

Project description: Not available

| S-EPMC12781752 | biostudies-literature

Titin-dependent transient ventricular defects result in adult atrial arrhythmia and impaired contractility

Project description:Atrial fibrillation (AF), the most common arrhythmia, is occasionally associated with cardiac developmental defects, but causal relationships are poorly defined. Importantly, functional compensation for developmental defects may mask increased risk of arrhythmia in adults. Here, we deleted 9 amino acids (Δ9) within a highly conserved A-band region of titin, a giant protein that serves as a molecular spring in cardiomyocytes, in both zebrafish and human induced pluripotent stem cell-derived atrial cardiomyocytes (hiPSC-aCMs). We find that the cardiac morphology of ttnaΔ9/Δ9 homozygous zebrafish embryos is perturbed and accompanied by reduced functional output, but ventricular function recovers within a few days of embryonic development, with most embryos reaching adulthood. Despite normal ventricular function, ttnaΔ9/Δ9 adults exhibit AF and atrial cardiomyopathy, with a striking absence of fibrosis, and these findings are recapitulated in TTNΔ9/Δ9-hiPSC-aCMs. Electrophysiological and proteomics analyses reveal atrial action potential shortening and increased expression and function of the cardiac potassium channel Kv7.1 and the slow delayed rectifier potassium current (IKs). Pharmacological suppression of IKs in both models prevents AF and improves atrial contractility. Collectively, these findings reveal how a small internal deletion in a large structural protein causes developmental abnormalities that functionally recover but increase the risk of adult cardiac disease via ion channel remodeling. The observed rescue with targeted antiarrhythmic therapy may have broader implications for the treatment of patients who harbor disease-causing rare variants in sarcomeric proteins.

2024-08-09 | PXD038300 | Pride

Proteomic profiles in cardiomyocytes exposed to ionizing radiation and resveratrol: potential radioprotective mechanisms of the different resveratrol pretreatment regimens

Project description:Resveratrol, a plant-derived antioxidant, may protect against radiation by modulating cellular metabolism and response to stress. Here, we explored its effects on human cardiomyocytes exposed to ionizing radiation. Resveratrol (5 µM) was administered for 1, 7, and 30 days before a single 2 Gy dose irradiation, and then radiation toxicity and changes in the proteome were evaluated. Extended resveratrol treatment (7 or 30 days) induced more profound proteomic changes than one-day treatment and partially counteracted toxic effects, leading to increased cell survival, reduced cell death, and fewer cells arrested in the G1 phase. Though resveratrol administration itself had a greater impact on the proteome than radiation alone, we identified three subsets of proteins differently affected by radiation depending on the resveratrol context. The first subset represented the core cellular response to radiation, unaffected by resveratrol. The second, linked to DNA repair, cell cycle checkpoints, and apoptosis, was affected by radiation only in the absence of resveratrol preconditioning, indicating the compound's protective effect. The third subset involved in metabolism regulation was affected by radiation only after extended resveratrol preconditioning. In conclusion, our data documented that the radioprotective effects of resveratrol are linked to a proteomic reprogramming of cardiomyocytes following prolonged exposure.

2025-11-10 | PXD069084 | Pride

Phytosterol accumulation results in ventricular arrhythmia, impaired cardiac function and death

Project description:Heart failure (HF) and cardiac arrhythmias share overlapping pathological mechanisms that act cooperatively to accelerate disease pathogenesis. Cardiac fibrosis is associated with both pathological conditions. Our previous work identified a link between phytosterol accumulation, cardiac fibrosis and death in a mouse model of phytosterolemia, a rare disorder characterized by elevated circulating phytosterols and increased cardiovascular disease risk. Here, we uncover a previously unknown pathological link between phytosterols and cardiac arrhythmias in the same animal model. Phytosterolemia resulted in inflammatory pathway induction, premature ventricular contractions (PVC) and ventricular tachycardia (VT). Both pharmacological and genetic inhibition of phytosterol absorption prevented the induction of both pathways. Inhibition of phytosterol absorption reduced inflammation and cardiac fibrosis, improved cardiac function, reduced the incidence of arrhythmias and increased survival in a mouse model of phytosterolemia. Collectively, this work identified a pathological mechanism whereby elevated phytosterols result in inflammation and cardiac fibrosis leading to impaired cardiac function, arrhythmias and sudden death. These phytosterolemia-associated comorbidities provide novel insight into the underlying pathophysiological mechanism that predispose these patients to increased risk of sudden cardiac death.

2021-08-31 | GSE173123 | GEO

Resveratrol action on A549 lung cancer cells

Project description:Resveratrol, a natural phytoestrogen found in red wine and a variety of plants, is reported to have protective effects against lung cancer, however there is very little work directed towards the understanding of the mechanism of action of resveratrol in lung cancer. In this study we used an experimental approach to understand the biological activity and molecular mechanisms of resveratrol in A549 lung cancer cells. Gene expression profiles were compiled using an oligonucleotide microarray to determine altered expression levels in resveratrol treated cells. Keywords: Genetic modification of A549 cells in response to resveratrol

2007-09-15 | GSE9008 | GEO

Effect of age, calorie restriction and resveratrol on gene expression in mouse heart, brain, and skeletal muscle

Project description:Resveratrol in high doses has been shown to extend lifespan in some studies in invertebrates and to prevent early mortality in mice fed a high-fat diet. We fed mice from middle age (14-months) to old age (30-months) either a control diet, a low dose of resveratrol (4.9 mg kg-1 day-1), or a calorie restricted (CR) diet and examined genome-wide transcriptional profiles. We report a striking transcriptional overlap of CR and resveratrol in heart, skeletal muscle and brain. Both dietary interventions inhibit gene expression profiles associated with cardiac and skeletal muscle aging. Gene expression profiling suggests that both CR and resveratrol may retard some aspects of aging through alterations in chromatin structure and transcription. Resveratrol, at doses that can be readily achieved in humans, fulfills the definition of a dietary compound that mimics some aspects of CR. Keywords: aging intervention study

2008-06-10 | GSE11291 | GEO

Transcription profiling of mouse heart, brain, and skeletal muscle to determine the rffect of age, calorie restriction and resveratrol on gene expression

2008-06-18 | E-GEOD-11291 | biostudies-arrayexpress

Phytosterol accumulation results in ventricular arrhythmia, impaired cardiac function and death

Project description:Phytosterol accumulation results in ventricular arrhythmia, impaired cardiac function and death

| PRJNA723851 | ENA

Deletion of Gja1 in myocardium emerges ventricular arrhythmia and tachycardia by reprogramming proline metabolism

Project description:Connexin43 (Cx43) is the predominant connexin in working myocardium. Its expression decreases in various cardiovascular diseases, and accompanied by ventricular arrhythmias (VAs). However, molecular mechanisms underlying increased arrhythmogenesis remained unclear. Here we established iPSC-derived cardiomyocytes (iPSC-CMs) and mouse models of Gja1 KO with proarrhythmic activity and disrupted proline metabolism. Mechanistically, Cx43 interacts with sodium-coupled neutral amino acid transporter 2 (SNAT2) where Gja1 KO reduces expression of SNAT2, leading to decreased proline and disrupted proline metabolism. Proline cycle in mitochondria preserves energetic/redox balance and exerts cardioprotective effects. Elevated reactive oxygen species (ROS) caused by disrupted proline metabolism leads to abnormal calcium handing and arrhythmia events. Taken together, the absence of Cx43 could facilitate the development of arrhythmias through reprogramming proline metabolism independent of reentry mechanisms, and indicated that molecular pathway of Cx43- SNAT2- ROS plays an essential role in maintaining normal cardiac rhythm.

2025-11-11 | MTBLS13302 | MetaboLights

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data