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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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Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
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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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The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
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Related Experiment Video

Updated: Dec 28, 2025

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
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Reductive Stress Causes Pathological Cardiac Remodeling and Diastolic Dysfunction.

Gobinath Shanmugam1, Ding Wang2, Sellamuthu S Gounder3

  • 1Cardiac Aging and Redox Signaling Laboratory, Division of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA.

Antioxidants & Redox Signaling
|February 18, 2020
PubMed
Summary
This summary is machine-generated.

Excessive antioxidant production causes reductive stress (RS), leading to heart failure. Blocking glutathione synthesis prevented RS and reversed cardiac damage, suggesting careful redox balance is crucial for heart health.

Keywords:
HCMiEFNrf2cardiac hypertrophydiastolic dysfunctionreductive stress

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Area of Science:

  • Cardiovascular Biology
  • Redox Biology
  • Molecular Cardiology

Background:

  • Redox homeostasis regulates cellular signaling, with antioxidant responses protecting against oxidative stress.
  • Excessive antioxidant generation can lead to detrimental reductive stress (RS).

Purpose of the Study:

  • To investigate how chronic reductive stress, driven by constitutive Nrf2 activation, promotes pathological cardiac remodeling.
  • To understand the long-term consequences of RS on heart function and survival.

Main Methods:

  • Utilized caNrf2 transgenic mice (TGL and TGH) to model chronic RS.
  • Assessed cardiac remodeling, ejection fraction, diastolic function, and survival rates.
  • Investigated the effect of pharmacologically inhibiting glutathione biosynthesis (using BSO) on RS and cardiac pathology.

Main Results:

  • Constitutive Nrf2 activation led to RS, increased glutathione redox potential, and pathological cardiac remodeling (hypertrophic cardiomyopathy) in TGH mice.
  • TGH mice showed significantly increased mortality and severe cardiac remodeling by 6 months, while TGL mice developed phenotypes later.
  • Early pharmacological blockade of glutathione synthesis prevented RS and rescued mice from cardiac remodeling and dysfunction.

Conclusions:

  • Chronic reductive stress is intolerable and sufficient to induce heart failure with diastolic dysfunction.
  • Sustained activation of antioxidant signaling pathways can drive pathological cardiac remodeling.
  • Therapeutic strategies for heart failure should carefully evaluate the redox state before initiating antioxidant treatments.