Related Experiment Video
Updated: Mar 3, 2026
Evaluation of Left Ventricular Structure and Function using 3D Echocardiography
Published on: October 28, 2020
In-depth proteomic profiling of left ventricular tissues in human end-stage dilated cardiomyopathy
Shanshan Liu1,2, Yan Xia3, Xiaohui Liu4
1Institutes of Biomedical Sciences of Shanghai Medical School and Minhang Hospital, Fudan University, Shanghai, China.
Insights
This study compared heart muscle proteins in dilated cardiomyopathy (DCM) patients and healthy individuals. Key differences in membrane proteins and cell death pathways were identified, offering new insights into DCM mechanisms.
Area of Science:
- Cardiology
- Proteomics
- Molecular Biology
Background:
- Dilated cardiomyopathy (DCM) is a primary cause of heart failure (HF) due to impaired left ventricular (LV) function.
- Understanding the molecular mechanisms of DCM is crucial for developing effective treatments.
Purpose of the Study:
- To profile the cardiac proteome in end-stage DCM using advanced mass spectrometry.
- To identify differentially expressed proteins and associated pathways in DCM.
- To validate key protein changes in human DCM samples.
Main Methods:
- iTRAQ-coupled 2D-LC-MS/MS was used to analyze LV tissue proteomes from DCM patients and healthy controls.
- Western blotting and multiple reaction monitoring (MRM) were employed for protein validation.
Main Results:
- 4263 proteins were identified, with 125 showing differential expression in DCM.
- Differentially expressed proteins were predominantly membrane proteins involved in cellular junctions, neuronal metabolism, and cell death.
- Activated cell death pathways and altered levels of S100A1 and eEF2 were confirmed in DCM tissues.
Conclusions:
- Proteomic analysis reveals significant alterations in cardiac proteins and pathways in end-stage DCM.
- Cell death activation and changes in specific proteins like S100A1 and eEF2 are implicated in DCM pathogenesis.
- These findings deepen the understanding of DCM mechanisms and may guide future therapeutic strategies.
Abstract:
Dilated cardiomyopathy (DCM) is caused by reduced left ventricular (LV) myocardial function, which is one of the most common causes of heart failure (HF). We performed iTRAQ-coupled 2D-LC-MS/MS to profile the cardiac proteome of LV tissues from healthy controls and patients with end-stage DCM. We identified 4263 proteins, of which 125 were differentially expressed in DCM tissues compared to LV controls. The majority of these were membrane proteins related to cellular junctions and neuronal metabolism. In addition, these proteins were involved in membrane organization, mitochondrial organization, translation, protein transport, and cell death process. Four key proteins involved in the cell death process were also detected by western blotting, indicated that cell death was activated in DCM tissues. Furthermore, S100A1 and eEF2 were enriched in the "cellular assembly and organization" and "cell cycle" networks, respectively. We verified decreases in these two proteins in end-stage DCM LV samples through multiple reaction monitoring (MRM). These observations demonstrate that our understanding of the mechanisms underlying DCM can be deepened through comparison of the proteomes of normal LV tissues with that from end-stage DCM in humans.
Related Concept Videos
01:30Cardiomyopathy II: Dilated Cardiomyopathy
01:29Cardiomyopathy III: Hypertrophic Cardiomyopathy
01:29Cardiomyopathy V: Interprofessional Care