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Related Concept Videos

Aortic Regurgitation II: Clinical Features and Diagnostic Tests01:22

Aortic Regurgitation II: Clinical Features and Diagnostic Tests

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Aortic valve regurgitation (AR) occurs when the aortic valve fails to close properly, allowing blood to flow backward from the aorta into the left ventricle. This backflow can result in two distinct clinical presentations: acute and chronic AR, each characterized by its own set of symptoms and physical findings.Acute Aortic RegurgitationAcute AR presents with a sudden onset of severe symptoms. Patients typically experience profound dyspnea (shortness of breath), chest pain, and signs of left...
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IntroductionAortic regurgitation is characterized by the backward flow of blood from the aorta into the left ventricle during diastole and arises from the improper closure of the aortic valve. This condition results in left ventricular volume overload and can stem from both acute and chronic etiologies, each contributing uniquely to the disease's progression and symptomatology.Acute and Chronic CausesAcute aortic regurgitation often results from events that suddenly impair the integrity of the...
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Aortic Regurgitation III: Medical Management01:25

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Aortic regurgitation (AR) is when the aortic valve does not close or seal properly, leading to backward blood circulation from the aorta into the left ventricle during diastole. Common causes of AR include rheumatic heart disease, congenital valve defects, and aortic root dilation. Managing AR requires a multifaceted approach to alleviate symptoms, preserve left ventricular function, and address the underlying cause of the regurgitation. Patients with symptomatic AR or significant left...
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Aneurysm I: Introduction01:30

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An aortic aneurysm is a localized outpouching or dilation at a weak point in the artery wall. It may involve different parts of the aorta, such as the abdominal aorta, aortic arch, or thoracic aorta.Etiological factorsSeveral disorders are associated with aortic aneurysms.Congenital causes, such as primary connective tissue disorders like Marfan syndrome, impact the integrity and strength of connective tissues, notably affecting the aorta. Marfan syndrome is a genetic disorder that specifically...
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Mitral Valve Prolapse I: Introduction01:27

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IntroductionThe mitral valve, one of the heart's four valves, regulates blood flow. These valves have flaps that open and close to direct blood properly through the heart and body. During each heartbeat, the flaps open for blood to pass through and seal shut to prevent backflow. Specifically, the mitral valve opens to allow blood flow from the heart's upper left chamber to the lower left chamber. It then closes securely as the lower left chamber contracts to pump blood to the body, preventing...
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Related Experiment Video

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Measurement of Pulse Propagation Velocity, Distensibility and Strain in an Abdominal Aortic Aneurysm Mouse Model
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Progressive Aortic Dilation Is Regulated by miR-17-Associated miRNAs.

Jie Wu1, Hui-Fang Song2, Shu-Hong Li3

  • 1Laboratory of Medical Genetics, Harbin Medical University, Harbin, China; Division of Cardiovascular Surgery, Toronto General Research Institute and Peter Munk Cardiac Centre, University Health Network, Toronto, Ontario, Canada; Department of Surgery, Division of Cardiac Surgery, University of Toronto, Toronto, Ontario, Canada.

Journal of the American College of Cardiology
|June 25, 2016
PubMed
Summary

MicroRNA-17 (miR-17) regulates tissue inhibitors of metalloproteinases (TIMPs) and matrix metalloproteinases (MMPs) in bicuspid aortic valve (BAV) patients, potentially initiating aortic dilation. Inhibiting miR-17 may prevent this progression.

Keywords:
MMPTIMPaortabicuspid aortic valve

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Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Genetics

Background:

  • Bicuspid aortic valve (BAV) patients face increased risk of aortic dilation due to extracellular matrix (ECM) degradation by matrix metalloproteinases (MMPs).
  • The initiating mechanisms of ECM degradation in BAV-associated aortic dilation remain unclear.
  • MicroRNA-17 (miR-17) regulates MMP activity in the heart by downregulating tissue inhibitors of metalloproteinases (TIMPs), suggesting a similar mechanism in the aorta.

Purpose of the Study:

  • To investigate if miR-17-related microRNA (miRNA) regulation of TIMP-MMP pathways drives aortic matrix degradation in BAV patients.
  • To elucidate the role of miR-17 in the early stages of aortic dilation in BAV.

Main Methods:

  • Comparative analysis of gene and protein expression in paired aortic tissues from BAV patients with varying dilation severity and normal controls.
  • In vitro studies using smooth muscle cells to assess the impact of miR-17 mimics and inhibitors on TIMP and MMP expression and activity.
  • Luciferase reporter assays to confirm direct regulation of TIMP-1 and TIMP-2 by miR-17.

Main Results:

  • Increased miR-17 expression was observed in less dilated BAV aortic tissue compared to severely dilated or normal tissue.
  • TIMP-1, -2, and -3 levels were decreased, while MMP2 activity was increased in less dilated BAV tissues, indicating early ECM degradation.
  • In vitro experiments demonstrated that miR-17 directly regulates TIMP-1 and TIMP-2 expression, influencing MMP2 activity.

Conclusions:

  • miR-17 directly controls TIMP-1 and TIMP-2 expression, impacting the TIMP-MMP balance in aortic tissue.
  • Less dilated BAV aortic tissue exhibits early-stage dilation driven by miR-17-related miRNAs.
  • Targeting miR-17 with inhibitory therapies presents a potential strategy to prevent aortic dilation in BAV patients.