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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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Autophagy01:27

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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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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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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
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In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells
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Autophagy and Heart Failure.

Jie Du1, Yan Liu2, Jintao Fu2

  • 1Beijing Anzhen Hospital Affiliated with Capital Medical University, Beijing, China. jiedubj@126.com.

Advances in Experimental Medicine and Biology
|July 17, 2020
PubMed
Summary
This summary is machine-generated.

Autophagic activity is present in heart failure, but its specific role remains unclear. This chapter explores macroautophagy and mitophagy in heart failure, detailing regulatory mechanisms.

Keywords:
AutophagyCardiac hypertrophyHeart failureMitochondrial autophagymicroRNA

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Area of Science:

  • Cardiovascular Biology
  • Cellular Stress Response
  • Molecular Medicine

Background:

  • Pressure overload is a known cause of cardiac hypertrophy and subsequent heart failure.
  • Autophagic processes, including macroautophagy and mitophagy, are observed in conditions of heart failure.
  • The precise contribution of autophagy to the progression or mitigation of heart failure is not fully elucidated.

Purpose of the Study:

  • To delineate the specific roles of macroautophagy and mitophagy in the context of heart failure.
  • To elucidate the molecular mechanisms that regulate autophagic activity during heart failure progression.

Main Methods:

  • Review of existing literature on autophagy in cardiac pathophysiology.
  • Analysis of studies investigating macroautophagy and mitophagy in heart failure models.
  • Examination of regulatory pathways impacting autophagic flux in the stressed heart.

Main Results:

  • Autophagy, encompassing both macroautophagy and mitophagy, is dynamically altered in heart failure.
  • Specific regulatory mechanisms influence the efficiency and outcome of these autophagic pathways.
  • Dysregulation of mitophagy may contribute to the accumulation of damaged mitochondria, exacerbating cardiac dysfunction.

Conclusions:

  • Autophagy plays a complex role in heart failure, with both potentially protective and detrimental aspects.
  • Understanding the regulation of macroautophagy and mitophagy is crucial for developing targeted therapeutic strategies for heart failure.
  • Further research into the precise molecular players is warranted to harness autophagy for cardiac repair.