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Related Concept Videos

Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

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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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Heart Failure II: Pathophysiology01:29

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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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A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
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Oxidative post-translational modifications develop LONP1 dysfunction in pressure overload heart failure.

Atsushi Hoshino1, Yoshifumi Okawa1, Makoto Ariyoshi1

  • 1From the Department of Cardiovascular Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan (A.H., Y.O., M.A., S.K., M.U., K.F., E.-I.K., S.M.); and the Department of Cardiovascular Medicine, Meiji University of Integrative Medicine, Kyoto, Japan (E.-I.K.).

Circulation. Heart Failure
|April 18, 2014
PubMed
Summary
This summary is machine-generated.

Mitochondrial AAA+ protease activity is reduced in heart failure due to oxidative damage. Restoring protease function improves heart energetics and contractility, suggesting a therapeutic target for heart failure.

Keywords:
heart failuremitochondriaprotein processing, post-translational

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Area of Science:

  • Cardiology
  • Mitochondrial Biology
  • Biochemistry

Background:

  • Mitochondrial dysfunction is a key factor in heart failure.
  • Cellular surveillance systems maintain mitochondrial integrity.
  • The role of mitochondrial AAA+ proteases in heart failure requires further investigation.

Purpose of the Study:

  • To evaluate the role of mitochondrial AAA+ protease in a mouse model of pressure overload heart failure.
  • To investigate the impact of oxidative modifications on protease activity.
  • To explore potential therapeutic interventions targeting mitochondrial proteases.

Main Methods:

  • Assessed ATP-dependent proteolytic activity in failing heart mitochondria using casein assays and immunoblotting.
  • Analyzed protein modifications, including cysteine reduction, tyrosine nitration, and carbonylation, in Lon protease homolog (LONP1).
  • Investigated the effects of mitochondria-targeted human catalase and mitoTEMPO on mitochondrial function and cardiac performance.

Main Results:

  • Heart failure mitochondria showed reduced proteolytic activity and increased oxidative damage to LONP1.
  • Electron transport chain protein levels accumulated due to decreased turnover.
  • Mitochondria-targeted catalase and mitoTEMPO improved mitochondrial energetics, respiration, and cardiac function.
  • LONP1 repression partially negated the protective effects of interventions.

Conclusions:

  • Oxidative modifications impair mitochondrial AAA+ protease activity, leading to electron transport chain dysfunction and heart failure.
  • Mitochondrial proteases are critical for maintaining protein homeostasis and cardiac function.
  • Targeting oxidatively inactivated proteases with agents like mitoTEMPO may be a viable treatment strategy for heart failure.