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Related Concept Videos

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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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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 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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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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Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
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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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Mitochondrial Function in Non-ischemic Heart Failure.

Anisha A Gupte1, Dale J Hamilton2,3

  • 1Center for Metabolism and Bioenergetics Research, Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX, USA. aagupte@houstonmethodist.org.

Advances in Experimental Medicine and Biology
|May 29, 2017
PubMed
Summary
This summary is machine-generated.

Heart failure involves mitochondrial dysfunction and metabolic stress, leading to energy depletion. Understanding these changes may help develop targeted therapies for non-ischemic heart failure.

Keywords:
CardiomyopathyHeart failureMitochondriaNon-ischemic

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Area of Science:

  • Cardiology
  • Mitochondrial Biology
  • Metabolic Disorders

Background:

  • The heart requires continuous energy supplied by mitochondria.
  • Non-ischemic cardiomyopathy, often due to pressure overload, causes metabolic stress and heart failure.
  • Mitochondria adapt to metabolic changes, but this can lead to contractile dysfunction.

Purpose of the Study:

  • To review mitochondrial functional changes in non-ischemic heart failure.
  • To explore potential therapeutic targets for preventing heart failure progression.
  • To discuss metabolism-targeted treatment options.

Main Methods:

  • Review of findings from animal models of non-ischemic heart failure.
  • Analysis of human studies on mitochondrial function in heart failure patients.
  • Examination of substrate supply pathways upstream of mitochondria.

Main Results:

  • Animal models consistently show cardiac mitochondrial dysfunction.
  • Human studies present inconsistent findings on mitochondrial dysfunction despite reduced ATP production.
  • Impaired substrate supply to mitochondria is a potential factor in heart failure.

Conclusions:

  • Mitochondrial dysfunction is implicated in non-ischemic heart failure.
  • Further research is needed to reconcile human and animal study findings.
  • Metabolism-targeted therapies hold promise for treating heart failure.