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Related Concept Videos

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...
Treatment for Pulmonary Arterial Hypertension: Phosphodiesterase Inhibitors01:28

Treatment for Pulmonary Arterial Hypertension: Phosphodiesterase Inhibitors

Phosphodiesterase 5 (PDE5) inhibitors are potent enzymes that function to hydrolyze cyclic nucleotides to their corresponding 5' monophosphates. Their unique biochemical properties have been applied in treating Pulmonary Arterial Hypertension (PAH).
Among the PDE5 inhibitors, sildenafil (Revatio) stands out as a competitive and selective inhibitor. It operates by elevating cellular levels of cGMP and augmenting signaling through the cGMP-PKG pathway, promoting vasodilation. Upon oral...
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...
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...
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers

Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
Diabetic Retinopathy01:27

Diabetic Retinopathy

DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...

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The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis
11:39

The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis

Published on: July 11, 2013

Retinoids and pulmonary hypertension.

Ioana R Preston1, Guangwen Tang, Jason U Tilan

  • 1Pulmonary, Critical Care and Sleep Division, Tufts-New England Medical Center, Tupper Research Institute, Boston, Mass, USA.

Circulation
|February 9, 2005
PubMed
Summary

Idiopathic pulmonary arterial hypertension patients have lower retinoic acid levels. Retinoic acid inhibits pulmonary artery smooth muscle cell growth, suggesting a role in pulmonary vascular remodeling.

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Establishment and Validation of a Rat Model of Pulmonary Arterial Hypertension Associated with Pulmonary Fibrosis
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Establishment and Validation of a Rat Model of Pulmonary Arterial Hypertension Associated with Pulmonary Fibrosis

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Isolation of Lung Retinoid-Containing Cells by Cell Sorting
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Isolation of Lung Retinoid-Containing Cells by Cell Sorting

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Last Updated: Jul 10, 2026

The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis
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Published on: July 11, 2013

Establishment and Validation of a Rat Model of Pulmonary Arterial Hypertension Associated with Pulmonary Fibrosis
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Isolation of Lung Retinoid-Containing Cells by Cell Sorting
07:47

Isolation of Lung Retinoid-Containing Cells by Cell Sorting

Published on: April 11, 2025

Area of Science:

  • Cardiovascular Research
  • Endocrinology
  • Cell Biology

Background:

  • Retinoic acid exhibits antimitogenic effects on smooth muscle cells, potentially reducing vascular thickening in systemic circulation.
  • The relationship between retinoids and pulmonary hypertension or pulmonary vascular remodeling remains unexplored.
  • This study investigates retinoid levels in idiopathic pulmonary arterial hypertension (IPAH) patients and retinoic acid's effects on pulmonary artery smooth muscle cells.

Purpose of the Study:

  • To determine retinoid levels in IPAH patients compared to healthy controls.
  • To investigate the impact of all-trans retinoic acid on human pulmonary artery smooth muscle cell proliferation.
  • To explore the potential role of retinoic acid in pulmonary vascular remodeling.

Main Methods:

  • Retinoid levels were quantified using gas chromatography-mass spectrometry in IPAH patients and controls.
  • Human pulmonary artery smooth muscle cells were cultured and treated with all-trans retinoic acid.
  • Retinoid acid receptor expression and gene array analysis (GADD45A) were performed.

Main Results:

  • IPAH patients showed significantly lower levels of all-trans retinoic acid and 13-cis retinoic acid.
  • All-trans retinoic acid suppressed serotonin-induced growth of human pulmonary artery smooth muscle cells.
  • Retinoic acid upregulated GADD45A expression, a known cell growth suppressor.

Conclusions:

  • IPAH patients exhibit reduced levels of retinoic acid.
  • Retinoic acid treatment induces growth-inhibitory signals in pulmonary artery smooth muscle cells in vitro.
  • Retinoic acid may play a role in the pathogenesis of pulmonary vascular remodeling in humans.