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Related Concept Videos

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...
Pulmonary Hypertension: Classification and Pathogenesis01:30

Pulmonary Hypertension: Classification and Pathogenesis

Pulmonary hypertension (PH) is a severe health condition in which the mean pulmonary arterial pressure increases to 25 mmHg or more, even when the body is at rest. This high pressure in the blood vessels that transport blood from the heart to the lungs can cause various symptoms, including shortness of breath, can lead to right heart failure, and significantly affect the overall quality of life.
There are various classifications for PH, each relating to different underlying causes and also...
Pulmonary Edema II: Pathophysiology01:18

Pulmonary Edema II: Pathophysiology

Pulmonary edema is the accumulation of fluid in the interstitial and alveolar spaces of the lungs, impairing gas exchange and oxygen delivery. It may be cardiogenic or noncardiogenic, but both reduce oxygenation and lung compliance.Cardiogenic Pulmonary EdemaCardiogenic edema results from increased hydrostatic pressure in pulmonary capillaries, usually due to left ventricular dysfunction from myocardial infarction, heart failure, or valvular disease. Ineffective cardiac pumping causes blood to...
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Chronic Obstructive Pulmonary Disease II: Emphysema01:23

Chronic Obstructive Pulmonary Disease II: Emphysema

Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.

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Related Experiment Video

Updated: Jul 1, 2026

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease
04:44

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Published on: June 16, 2020

Endothelin and scleroderma lung disease.

R M Silver1

  • 1Division of Rheumatology and Immunology, Medical University of South Carolina, Charleston, SC 29425, USA. silverr@musc.edu

Rheumatology (Oxford, England)
|September 17, 2008
PubMed
Summary
This summary is machine-generated.

Scleroderma-associated interstitial lung disease (SSc-ILD) involves lung fibrosis. Endothelin-1 (ET-1) may drive SSc-ILD, but trials of ET receptor blockers like bosentan showed limited efficacy.

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A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats
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A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats

Published on: March 1, 2022

Area of Science:

  • Pulmonary Medicine
  • Rheumatology
  • Cell Biology

Background:

  • Scleroderma-associated interstitial lung disease (SSc-ILD) is a frequent and fatal complication of scleroderma.
  • It often presents as non-specific interstitial pneumonia, potentially leading to pulmonary fibrosis.
  • Fibrosis results from fibroblast proliferation and extracellular matrix deposition.

Purpose of the Study:

  • To investigate the role of Endothelin-1 (ET-1) in the pathogenesis of SSc-ILD.
  • To evaluate the efficacy of ET receptor blockers in treating SSc-ILD.

Main Methods:

  • Review of in vitro and in vivo studies on ET-1 in SSc-ILD.
  • Analysis of data from two randomized controlled trials of the dual ET receptor blocker bosentan.

Main Results:

  • ET-1 may mediate SSc-ILD by promoting pulmonary mesenchymal cell proliferation and enhancing TGF-beta's fibrogenic effects.
  • Bosentan trials did not meet primary or secondary endpoints for SSc-ILD, despite potential explanations for lack of efficacy.

Conclusions:

  • ET-1 is a potential central mediator in SSc-ILD pathogenesis.
  • Further research is needed to understand the efficacy of ET receptor blockers in SSc-ILD.
  • Investigating alternative therapeutic strategies for SSc-ILD is crucial.