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

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
COPD: Pathogenesis and Clinical Features01:20

COPD: Pathogenesis and Clinical Features

2.0K
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...
2.0K
Chronic Obstructive Pulmonary Disease-III: Symptoms and Complications.01:25

Chronic Obstructive Pulmonary Disease-III: Symptoms and Complications.

4.0K
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:
4.0K
Chronic Obstructive Pulmonary Disease01:24

Chronic Obstructive Pulmonary Disease

2.8K
COPD is defined as a heterogeneous lung condition marked by persistent respiratory symptoms such as dyspnea, cough, and sputum production, caused by abnormalities in the airways that cause airflow obstruction.
Smoking is a primary risk factor for COPD, with over 80% of patients having a history of it. Patients typically experience progressive dyspnea or labored breathing, frequent coughing, and recurrent pulmonary infections. Many eventually succumb to respiratory failure, characterized by...
2.8K
Chronic Obstructive Pulmonary Disease-I: Introduction01:20

Chronic Obstructive Pulmonary Disease-I: Introduction

4.0K
Chronic Obstructive Pulmonary Disease (COPD) is a long-lasting respiratory condition requiring continuous attention and care. It is a progressive lung disease that leads to breathing challenges due to airflow obstruction. It manifests as persistent respiratory symptoms and restricted airflow resulting from abnormalities in the airways and alveoli, usually due to long-term exposure to harmful particles or gases. COPD mainly consists of two primary conditions: emphysema and chronic bronchitis.
4.0K
COPD: Management Using Bronchodilators and Corticosteroids01:26

COPD: Management Using Bronchodilators and Corticosteroids

958
Chronic obstructive pulmonary isease (COPD) involves a group of progressive lung disorders characterized by persistent airflow limitation and chronic respiratory symptoms. Asthma-COPD Overlap Syndrome (ACOS), encompassing features of both asthma and Chronic obstructive pulmonary disease (COPD), is a group of progressive lung disorders that includes chronic bronchitis, emphysema, and refractory (non-reversible) asthma. ACOS leads to complex clinical presentations that combine the inflammatory...
958

You might also read

Related Articles

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

Sort by
Same author

Kirenol alleviates Th2-driven allergic asthma by modulating T-cell responses.

International immunopharmacology·2026
Same author

Central precocious puberty and risk of atopic diseases: The mediating role of obesity and sex hormones.

Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology·2026
Same author

Extreme temperature and airway dehydration: current understanding and integrative insights into respiratory vulnerability.

Expert review of respiratory medicine·2026
Same author

Long-term ambient temperature and asthma severity and hospitalization in children: a population-based study.

European journal of pediatrics·2026
Same author

Hippo signaling pathway regulates branching morphogenesis of the fetal lung under hypoxia.

Pediatric research·2026
Same author

Assessing the impact of air pollution on anemia: a comprehensive review and meta-analysis.

Expert review of hematology·2026

Related Experiment Video

Updated: Mar 3, 2026

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma
10:21

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma

Published on: September 20, 2024

935

SUV39H1 Reduction Is Implicated in Abnormal Inflammation in COPD.

Tzu-Tao Chen1,2, Sheng-Ming Wu1, Shu-Chuan Ho1,3

  • 1Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.

Scientific Reports
|April 21, 2017
PubMed
Summary
This summary is machine-generated.

SUV39H1 levels are reduced in chronic obstructive pulmonary disease (COPD), leading to increased inflammation. Restoring SUV39H1 may offer a new therapeutic strategy for COPD patients.

More Related Videos

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice
10:37

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice

Published on: January 16, 2015

13.7K
Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
08:17

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure

Published on: August 25, 2017

11.6K

Related Experiment Videos

Last Updated: Mar 3, 2026

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma
10:21

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma

Published on: September 20, 2024

935
Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice
10:37

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice

Published on: January 16, 2015

13.7K
Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
08:17

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure

Published on: August 25, 2017

11.6K

Area of Science:

  • Epigenetics
  • Pulmonary Medicine
  • Molecular Biology

Background:

  • Chronic obstructive pulmonary disease (COPD) involves persistent inflammation in airways and lungs.
  • SUV39H1, a histone methyltransferase, plays a role in epigenetic regulation.
  • Abnormal inflammation is a hallmark of COPD pathology.

Purpose of the Study:

  • To investigate the causal role of SUV39H1 in COPD-associated inflammation.
  • To explore the epigenetic mechanisms linking SUV39H1 to COPD pathogenesis.
  • To identify SUV39H1 as a potential therapeutic target for COPD.

Main Methods:

  • Measured SUV39H1 and H3K9me3 levels in patient samples (PBMCs, HSAEpCs, lung tissue).
  • Utilized a SUV39H1 inhibitor (chaetocin) in cell and animal models.
  • Performed SUV39H1 knockdown and overexpression experiments.
  • Analyzed inflammatory cytokine profiles and chromatin modifications.

Main Results:

  • Reduced SUV39H1 and H3K9me3 levels in COPD patients correlated with disease severity.
  • SUV39H1 inhibition mimicked COPD inflammation by affecting IL-8 promoter activity.
  • SUV39H1 modulation (knockdown/overexpression) directly impacted COPD-related inflammation.
  • Inhibition of SUV39H1 exacerbated inflammation in COPD mouse models.

Conclusions:

  • SUV39H1 epigenetically regulates pro-inflammatory cytokines.
  • Reduced SUV39H1 in COPD causes loss of H3K9me3, promoting inflammation.
  • SUV39H1 and its pathways represent promising therapeutic targets for COPD.