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Related Concept Videos

Heart Failure I: Introduction01:27

Heart Failure I: Introduction

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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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Pathophysiology of Heart Failure01:17

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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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Imbalances in Cardiac Output01:26

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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.
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send...
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Mitral Regurgitation I: Introduction01:20

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Mitral regurgitation is characterized by the backward circulation of blood from the left ventricle to the left atrium during systole, a phase of the cardiac cycle when the heart contracts and pumps blood out of the chambers. This abnormal flow occurs primarily due to the dysfunction of the mitral valve or its supporting structures, which include the mitral leaflets, chordae tendineae, annulus, and papillary muscles.Etiology and Mechanisms:Primary Mitral Regurgitation: This type arises from...
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Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

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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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Mitral Stenosis I: Introduction01:22

Mitral Stenosis I: Introduction

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Mitral Valve Stenosis (MVS) is a heart condition where the mitral valve narrows, impeding blood circulation from the left atrium to the left ventricle. The etiology and pathophysiology of this condition are multifaceted, leading to a cascade of cardiovascular complications.Causes of Mitral Valve StenosisRheumatic Heart Disease: It is the main cause of mitral valve stenosis, particularly in developing nations. This condition arises from rheumatic fever, an inflammatory illness resulting from...
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BubR1 Insufficiency Drives Transcriptomic Alterations and Pathology Associated With Cardiac Aging and Heart Failure.

Renju Pun1, Aliya L Haas1, Aradhana Thapa1

  • 1Department of Biomedical Sciences, School of Medicine, Creighton University, Omaha, Nebraska, USA.

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Reduced BubR1 protein levels accelerate cardiac aging and heart failure by promoting hypertrophy and fibrosis. Maintaining BubR1 may protect against age-related heart disease and improve elderly heart health.

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Area of Science:

  • Cardiovascular Biology
  • Aging Research
  • Molecular Cardiology

Background:

  • Aging is a primary risk factor for heart disease, causing pathological changes like hypertrophy, fibrosis, and senescence.
  • BubR1 ( a protein kinase involved in cell cycle and chromosome stability) is linked to systemic aging, but its role in cardiac aging is not well understood.

Purpose of the Study:

  • To investigate the role of BubR1 in regulating cardiac aging and its contribution to heart disease pathogenesis.
  • To explore BubR1's potential as a therapeutic target for age-related cardiac dysfunction.

Main Methods:

  • Investigated BubR1 insufficiency in mouse models.
  • Performed transcriptomic profiling of hearts from BubR1-deficient mice and compared them to aged hearts and human heart failure samples.
  • Examined BubR1 expression in aging hearts, heart failure models, and human heart failure patients.
  • Studied the effects of BubR1 reduction in isolated cardiomyocytes.

Main Results:

  • BubR1 insufficiency in mice led to cardiac hypertrophy, fibrosis, and cellular senescence.
  • Transcriptomic analysis revealed disrupted pathways in cardiac function and shared gene networks with aged hearts.
  • BubR1 levels decline with age and are reduced in heart failure patients and models.
  • Reduced BubR1 in cardiomyocytes increased markers of heart failure, hypertrophy, and cytoskeletal remodeling.

Conclusions:

  • BubR1 deficiency is associated with cardiac aging and heart failure in humans.
  • Sustaining BubR1 expression may be a therapeutic strategy to combat age-related cardiac decline and improve heart health.