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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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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...
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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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Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
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β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
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GRSF1 Protects Against Heart Failure by Maintaining BCAA Homeostasis.

Hu Wang1, Jiaxing Wang1, Min Zhu1,2

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Summary

The RNA-binding protein GRSF1 is crucial for maintaining heart health by regulating branched-chain amino acid (BCAA) metabolism. Loss of GRSF1 leads to heart failure, while its preservation offers therapeutic potential for cardiometabolic diseases.

Keywords:
BCAA metabolismGRSF1RNA-binding proteinheart failure

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Metabolic Regulation

Background:

  • Cardiac branched-chain amino acid (BCAA) metabolism and mitochondrial dysfunction are linked to heart failure.
  • The precise mechanisms causing reduced BCAA metabolism in heart failure are not fully understood.

Purpose of the Study:

  • To investigate the role of the RNA-binding protein GRSF1 in cardiac BCAA metabolism and heart failure pathogenesis.
  • To elucidate the molecular mechanisms by which GRSF1 influences BCAA homeostasis and mitochondrial function.

Main Methods:

  • Examined GRSF1 expression in human heart failure tissues and generated genetically modified mice (cardiomyocyte-specific GRSF1 deletion/overexpression).
  • Utilized metabolomics and mitochondrial function assays to assess GRSF1's impact on BCAA homeostasis.
  • Investigated the interaction between GRSF1 and BCKDHB mRNA using specific mouse models.

Main Results:

  • GRSF1 levels were decreased in failing human and mouse hearts.
  • GRSF1 deficiency caused cardiac dysfunction, dilated cardiomyopathy, hypertrophy, and fibrosis.
  • GRSF1 overexpression protected against heart failure, maintaining BCAA homeostasis and mitochondrial function by stabilizing BCKDHB mRNA.
  • Functional recovery from GRSF1 overexpression was dependent on BCKDHB.

Conclusions:

  • GRSF1 acts as a critical cell-intrinsic metabolic checkpoint in the heart.
  • GRSF1 maintains cardiac BCAA homeostasis by regulating BCKDHB mRNA turnover.
  • Targeting GRSF1 presents a potential therapeutic strategy for heart failure and related cardiometabolic diseases.