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 III: Chronic Bronchitis Features01:24

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

2
Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...
2
Pneumonia I: Introduction01:29

Pneumonia I: Introduction

1
Pneumonia is an infection of the lower respiratory tract that leads to inflammation of the lung parenchyma, often resulting in the accumulation of inflammatory exudate in the alveoli and airways. Unlike the watery, low-protein fluid exudate in pulmonary edema, the exudate in this case is a thick fluid rich in immune cells, proteins, and debris produced during infection and inflammation.This impairs gas exchange and can lead to consolidation of lung tissue. The infection may be caused by a...
1
Chronic Obstructive Pulmonary Disease II: Emphysema01:23

Chronic Obstructive Pulmonary Disease II: Emphysema

2
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.
2
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

5.3K
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
5.3K
Atelectasis II: Pathophysiology01:10

Atelectasis II: Pathophysiology

2
Atelectasis develops when alveoli lose their air and collapse inward. Because lung tissue is naturally elastic, these air sacs shrink rather than remaining open. Collapsed alveoli are no longer ventilated, reducing their role in gas exchange. Blood flow may continue in these regions, creating a ventilation–perfusion mismatch. Clinical findings include decreased breath sounds, dullness to percussion, reduced chest expansion, and decreased tactile fremitus as sound transmission through...
2
COPD: Pathogenesis and Clinical Features01:20

COPD: Pathogenesis and Clinical Features

2.2K
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...
2.2K

You might also read

Related Articles

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

Sort by
Same author

Opportunities for Human Lung Tissue-Based Studies in Fibrotic ILD Research.

American journal of respiratory and critical care medicine·2026
Same author

Monocyte-Derived LGMN<sup>+</sup> Macrophages Divert Lung Injury Outcomes toward Fibrosis through Matrix Remodeling.

Research (Washington, D.C.)·2026
Same author

Nintedanib in Post-COVID Interstitial Lung Disease: a double-blind, randomized, placebo-controlled Clinical Trial.

Annals of the American Thoracic Society·2026
Same author

Early Pulmonary Fibrosis is Defined by Niche- and Cell-Specific Molecular Programs.

bioRxiv : the preprint server for biology·2026
Same author

Occupational inhaled exposures and risk of interstitial lung abnormalities in individuals with potential familial susceptibility to pulmonary fibrosis.

Thorax·2026
Same author

Macropinocytosis inhibition attenuates profibrotic responses in lung fibroblasts and pulmonary fibrosis models.

The Journal of clinical investigation·2026

Related Experiment Video

Updated: Apr 18, 2026

Refined Murine Model of Idiopathic Pulmonary Fibrosis
07:51

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Published on: June 17, 2025

1.4K

Update in diffuse parenchymal lung disease, 2013.

Ivan O Rosas1, Naftali Kaminski

  • 11 Division of Pulmonary and Critical Care, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.

American Journal of Respiratory and Critical Care Medicine
|January 31, 2015
PubMed
Summary
This summary is machine-generated.

Idiopathic pulmonary fibrosis (IPF) research has advanced significantly with genetic discoveries and new biomarkers. Two drugs, pirfenidone and nintedanib, have now been FDA-approved for slowing IPF progression.

Keywords:
ILDIPFgenomicsimmunitypersonalized medicine

More Related Videos

Unilateral Lung Volume Analysis Using Micro-CT for Enhanced Assessment of Pulmonary Fibrosis in Preclinical Models
03:38

Unilateral Lung Volume Analysis Using Micro-CT for Enhanced Assessment of Pulmonary Fibrosis in Preclinical Models

Published on: June 20, 2025

1.2K
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

21.2K

Related Experiment Videos

Last Updated: Apr 18, 2026

Refined Murine Model of Idiopathic Pulmonary Fibrosis
07:51

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Published on: June 17, 2025

1.4K
Unilateral Lung Volume Analysis Using Micro-CT for Enhanced Assessment of Pulmonary Fibrosis in Preclinical Models
03:38

Unilateral Lung Volume Analysis Using Micro-CT for Enhanced Assessment of Pulmonary Fibrosis in Preclinical Models

Published on: June 20, 2025

1.2K
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

21.2K

Area of Science:

  • Pulmonary Medicine
  • Genetics
  • Pharmacology

Background:

  • Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease with limited treatment options.
  • Recent research has focused on identifying genetic factors and molecular biomarkers associated with IPF.
  • Understanding disease mechanisms is crucial for developing effective therapies.

Purpose of the Study:

  • To summarize key advances in idiopathic pulmonary fibrosis (IPF) research.
  • To highlight the identification of genetic variants and biomarkers in IPF.
  • To discuss the clinical implications of recent drug approvals for IPF treatment.

Main Methods:

  • Review of recent scientific literature and clinical trial data.
  • Analysis of genetic association studies and biomarker discovery in IPF.
  • Evaluation of the impact of pirfenidone and nintedanib on IPF progression.

Main Results:

  • Identification of genetic variants linked to IPF in a significant patient population.
  • Discovery of molecular and genetic biomarkers predicting IPF clinical phenotypes and biological pathways.
  • Confirmation that pirfenidone and nintedanib slow disease progression in IPF patients.

Conclusions:

  • Recent advances in IPF research, including genetic insights and biomarker discoveries, have paved the way for targeted therapies.
  • The FDA approval of pirfenidone and nintedanib marks a historic milestone in managing IPF.
  • Future research directions include further exploration of biological mechanisms and personalized treatment strategies for IPF.