Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Pulmonary Hypertension: Classification and Pathogenesis01:30

Pulmonary Hypertension: Classification and Pathogenesis

702
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...
702
Treatment for Pulmonary Arterial Hypertension: Phosphodiesterase Inhibitors01:28

Treatment for Pulmonary Arterial Hypertension: Phosphodiesterase Inhibitors

646
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...
646
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

550
Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
550
COPD: Pathogenesis and Clinical Features01:20

COPD: Pathogenesis and Clinical Features

1.9K
Chronic obstructive pulmonary disease (COPD) is a group of lung conditions that progressively worsen over time, including chronic bronchitis and emphysema. This cluster of diseases collectively leads to a gradual and irreversible decline in lung function over time.
The primary cause for the onset of COPD is cigarette smoking and exposure to air pollution. These hazardous factors initiate a chain reaction within the lungs, resulting in chronic inflammation, damage to the airways, and a...
1.9K
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

4.9K
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
4.9K
Chronic Obstructive Pulmonary Disease-III: Symptoms and Complications.01:25

Chronic Obstructive Pulmonary Disease-III: Symptoms and Complications.

3.9K
Understanding the variety of primary symptoms and systemic complications that characterize chronic obstructive pulmonary disease (COPD) is crucial for healthcare professionals.
Symptoms of COPD can be classified as primary or systemic. Primary symptoms relate to reduced airflow, while systemic or extrapulmonary symptoms relate to COPD's broader impact on the body.
Primary Symptoms of COPD:
3.9K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Clinical, biological and cytometric characteristics of two patients with a homozygous A91V<i>PRF1</i> mutation.

Clinical & translational immunology·2026
Same author

Occupational category, job type, and sarcoidosis: Findings from a French multicenter study.

Pulmonology·2026
Same author

The IL-10/IL-6 Ratio and the Risk Score: Two Cytokines-Based Predictors for Malignancy-Associated Hemophagocytic Lymphohistiocytosis in Adults (M-HLHa).

American journal of hematology·2026
Same author

Intensive care admissions for severe immune-related adverse events associated with immune checkpoint inhibitor therapy: a 10-year cohort study.

Journal of critical care·2026
Same author

Factors associated with variations in the 6-minute walk distance during the follow-up of patients with systemic sclerosis.

Arthritis research & therapy·2026
Same author

Beyond screening for pulmonary arterial hypertension: The DETECT score is a potential promising prediction tool for all-cause mortality in systemic sclerosis: Analysis from the EUSTAR database.

Journal of autoimmunity·2026

Related Experiment Video

Updated: Feb 22, 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

20.9K

Pulmonary hypertension in systemic sclerosis: different phenotypes.

David Launay1,2,3,4, Vincent Sobanski5,2,3,4, Eric Hachulla5,2,3,4

  • 1Lille Inflammation Research International Center (LIRIC), UMR 995, Université de Lille, Lille, France david.launay@univ-lille2.fr.

European Respiratory Review : an Official Journal of the European Respiratory Society
|September 29, 2017
PubMed
Summary
This summary is machine-generated.

Pulmonary hypertension (PH) in systemic sclerosis (SSc) presents diverse causes, including lung disease and heart dysfunction. Accurate phenotyping is crucial for effective treatment of SSc-PH.

More Related Videos

Increasing Pulmonary Artery Pulsatile Flow Improves Hypoxic Pulmonary Hypertension in Piglets
08:08

Increasing Pulmonary Artery Pulsatile Flow Improves Hypoxic Pulmonary Hypertension in Piglets

Published on: May 11, 2015

14.7K
Left Atrial Stenosis Induced Pulmonary Venous Arterialization and Group 2 Pulmonary Hypertension in Rat
08:34

Left Atrial Stenosis Induced Pulmonary Venous Arterialization and Group 2 Pulmonary Hypertension in Rat

Published on: November 18, 2018

7.7K

Related Experiment Videos

Last Updated: Feb 22, 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

20.9K
Increasing Pulmonary Artery Pulsatile Flow Improves Hypoxic Pulmonary Hypertension in Piglets
08:08

Increasing Pulmonary Artery Pulsatile Flow Improves Hypoxic Pulmonary Hypertension in Piglets

Published on: May 11, 2015

14.7K
Left Atrial Stenosis Induced Pulmonary Venous Arterialization and Group 2 Pulmonary Hypertension in Rat
08:34

Left Atrial Stenosis Induced Pulmonary Venous Arterialization and Group 2 Pulmonary Hypertension in Rat

Published on: November 18, 2018

7.7K

Area of Science:

  • Cardiology
  • Pulmonology
  • Rheumatology

Background:

  • Pulmonary hypertension (PH) is a severe complication of systemic sclerosis (SSc).
  • PH in SSc is heterogeneous due to SSc phenotypes and varied PH mechanisms.
  • PH causes in SSc include pulmonary arterial hypertension, lung disease, and left-heart disease.

Purpose of the Study:

  • To review and clarify the different phenotypes of PH in systemic sclerosis (SSc-PH).
  • To highlight the importance of differentiating SSc-PH causes for tailored therapy.

Main Methods:

  • Literature review of SSc-PH phenotypes.
  • Analysis of PH classification groups relevant to SSc.
  • Discussion of diagnostic challenges in SSc-PH.

Main Results:

  • SSc-PH can stem from small artery vasculopathy (Group 1), lung disease (Group 3), or cardiac dysfunction (Group 2).
  • Pulmonary veno-occlusive disease (Group 1') also contributes to PH in SSc.
  • Distinguishing the dominant PH cause in SSc patients is often challenging.

Conclusions:

  • Understanding SSc-PH phenotypes is essential for appropriate management.
  • Therapeutic strategies for SSc-PH differ significantly based on the underlying cause.
  • This review aims to aid in deciphering the complex phenotypes of SSc-PH.