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Related Concept Videos

Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

4.8K
Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
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Heart Failure I: Introduction01:27

Heart Failure I: Introduction

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Heart failure refers to a clinical syndrome caused by structural or functional cardiac disorders that prevent the heart from pumping an adequate amount of blood to meet the body's metabolic needs. This condition often arises from myocardial infarction or ischemia, leading to decreased cardiac output, reduced tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability.Heart failure can result from disruptions in the mechanisms that regulate cardiac output...
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Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

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Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
1.9K
Heart Failure IV: Classification and Diagnostic Evaluation01:30

Heart Failure IV: Classification and Diagnostic Evaluation

1.0K
Heart failure can be classified in various ways, with the most common classifications based on physical activity limitations, disease progression, severity, and treatment strategies.The Functional Classification of Heart Failure divides patients into four categories based on physical activity limitation due to symptom burden.Class I: Patients in this class have cardiac disease but no physical activity limitations. Ordinary activities like walking, climbing stairs, or routine tasks do not cause...
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Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

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Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
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Quantitative Analysis of Chromatin Proteomes in Disease
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Deciphering heart failure: an integrated proteomic and transcriptomic approach with experimental validation.

Jun Cao1, Zhaohai Su1, Bilong Zhang1

  • 1Department of Cardiology, Ganzhou Hospital of Guangdong Provincial People's Hospital, Ganzhou Municipal Hospital (Gannan Medical University Affiliated Municipal Hospital), 49 Dagong Road, 341000, Ganzhou, China.

Functional & Integrative Genomics
|October 23, 2024
PubMed
Summary

Heart failure (HF) involves molecular changes, particularly increased Acyl-CoA synthetase long-chain family member 4 (ACSL4). Targeting ACSL4 to inhibit ferroptosis shows promise as a novel therapeutic strategy for HF.

Keywords:
ACSL4Heart failureMulti-omics analysis

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Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Biochemistry

Background:

  • Heart failure (HF) is a complex syndrome characterized by significant molecular alterations.
  • Ferroptosis, a regulated form of cell death, is increasingly recognized for its role in cardiovascular disease pathogenesis.

Purpose of the Study:

  • To identify key molecular changes in heart failure using multi-omics data.
  • To investigate the therapeutic potential of targeting ferroptosis, specifically the protein ACSL4, in HF.

Main Methods:

  • Analysis of transcriptomic and proteomic data from human HF samples and a HF mouse model.
  • Cross-analysis of differentially expressed genes (DEGs) and proteins.
  • Functional validation using a hypoxia-induced ischemia model in HL-1 cardiomyocytes with ACSL4 knockdown.

Main Results:

  • Multi-omics analysis revealed significant enrichment in immune, inflammatory, and metabolic pathways in HF.
  • ACSL4 expression was consistently upregulated at both transcriptional and protein levels in HF.
  • In vitro, ACSL4 knockdown suppressed ferroptosis, reduced oxidative stress markers (ROS, MDA, free iron), and improved cardiomyocyte viability.

Conclusions:

  • Increased ACSL4 expression is a key molecular event in heart failure.
  • Targeting ACSL4 to inhibit ferroptosis presents a potential novel therapeutic strategy for treating heart failure.