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Related Concept Videos

Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Esophageal Varices-I: Introduction01:24

Esophageal Varices-I: Introduction

Esophageal varices are dilated, tortuous veins which are found mainly in the submucosa of the lower esophagus but which may also appear higher up or extend into the stomach. They develop due to increased pressure in the portal venous system, often as a result of liver cirrhosis. This condition scars and damages the liver, impeding normal blood flow through the portal vein. To compensate, blood seeks alternative pathways, forming fragile new vessels (varices) in the esophagus and stomach. These...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Esophageal Varices-II: Clinical Features and Management01:28

Esophageal Varices-II: Clinical Features and Management

Esophageal varices often manifest as gastrointestinal bleeding episodes, presenting symptoms like hematemesis (vomiting of blood), hematochezia (passing fresh blood via the rectum), and melena (black, tarry stools). Other signs can include weight loss, anorexia, abdominal discomfort, jaundice, pruritus, altered mental status, and muscle cramps.
In the initial assessment, a thorough review of the patient's medical history is vital to identify risk factors such as liver disease, alcohol abuse, or...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Portal Hypertension01:22

Portal Hypertension

Portal hypertension is an increase in blood pressure within the portal venous system. Normally, this pressure is less than 5 mmHg. It is considered clinically significant when it rises above 10 mmHg. At this threshold, complications from altered blood flow and venous congestion emerge.EtiologyPortal hypertension arises from conditions that impede blood flow through the liver. The most common cause is cirrhosis, in which chronic liver injury leads to fibrotic scarring. This fibrosis narrows or...

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Related Experiment Video

Updated: May 13, 2026

In Vitro Three-Dimensional Sprouting Assay of Angiogenesis Using Mouse Embryonic Stem Cells for Vascular Disease Modeling and Drug Testing
08:04

In Vitro Three-Dimensional Sprouting Assay of Angiogenesis Using Mouse Embryonic Stem Cells for Vascular Disease Modeling and Drug Testing

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[Hereditary hemorrhagic telangiectasia].

P Duffau1, E Lazarro2, J-F Viallard2

  • 1Service de médecine interne, hôpital Saint-André, CHU de Bordeaux, 1, rue Jean-Burguet, 33000 Bordeaux, France.

La Revue De Medecine Interne
|March 23, 2013
PubMed
Summary

Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome) is an underdiagnosed vascular disorder. Understanding its genetic basis and clinical patterns is key for effective management and potential angiogenesis-based therapies.

Keywords:
AngiogenesisAngiogenèseArteriovenous malformationsHereditary hemorrhagic telangiectasiaMaladie de Rendu-OslerMalformation artério-veineuseMonogenic diseaseTransmission autosomique dominanteÉpistaxis

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Last Updated: May 13, 2026

In Vitro Three-Dimensional Sprouting Assay of Angiogenesis Using Mouse Embryonic Stem Cells for Vascular Disease Modeling and Drug Testing
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Area of Science:

  • Vascular Biology
  • Genetics
  • Medical Genetics

Background:

  • Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome) is a common yet underdiagnosed monogenic vascular disorder.
  • Characterized by telangiectases and arteriovenous malformations, its subtle early signs include nosebleeds and visible vascular lesions.

Purpose of the Study:

  • To summarize the genetic basis and clinical presentation of hereditary hemorrhagic telangiectasia.
  • To emphasize the importance of understanding vascular malformation patterns for optimal patient management.
  • To explore the potential of anti-angiogenesis therapies.

Main Methods:

  • Review of genetic mutations associated with hereditary hemorrhagic telangiectasia.
  • Analysis of clinical features and diagnostic challenges.
  • Discussion of therapeutic strategies, including angiogenesis modulation.

Main Results:

  • Mutations in ENG and ACVRL1/ALK1 genes account for approximately 85% of hereditary hemorrhagic telangiectasia cases.
  • Clinical manifestations, such as epistaxis and mucocutaneous telangiectases, are often subtle.
  • Optimal management necessitates detailed knowledge of vascular malformation characteristics.

Conclusions:

  • Hereditary hemorrhagic telangiectasia requires increased diagnostic awareness due to its prevalence and subtle initial symptoms.
  • Genetic factors, particularly mutations in ENG and ACVRL1/ALK1, are central to the disorder.
  • Targeting angiogenesis presents a promising therapeutic avenue for managing vascular malformations in hereditary hemorrhagic telangiectasia.