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

Treatment for Pulmonary Arterial Hypertension: Oxygen Therapy for Respiratory Failure01:16

Treatment for Pulmonary Arterial Hypertension: Oxygen Therapy for Respiratory Failure

Oxygen therapy has emerged as a significant tool in enhancing the quality of life for patients suffering from pulmonary arterial hypertension (PAH). While this therapy has principally been studied on patients with significant hypoxemia, this therapeutic approach helps prevent potential organ damage and can be administered in the comfort of one's home.
Oxygen therapy is vital in increasing and maintaining blood oxygen levels in PAH patients. As a result, it aids in reducing fatigue, improving...
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
Cystic Fibrosis: Management01:24

Cystic Fibrosis: Management

Cystic fibrosis (CF) is an autosomal recessive disorder that predominantly affects individuals of Northern European descent, occurring at a rate of 1 in 3500. It is caused by a genetic mutation in a gene on chromosome 7, most commonly the ΔF508 mutation, that codes for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. This results in thicker mucus secretions and obstruction pathologies in multiple organs, including the lungs and sinuses.
Sinus disease and chronic sinusitis...
Antiasthma Drugs: Leukotriene Modifiers01:19

Antiasthma Drugs: Leukotriene Modifiers

Leukotriene modifiers, or cysteinyl leukotriene receptor antagonists, are medications used to manage chronic asthma. These agents target specific inflammatory mediators produced during arachidonic acid metabolism, an essential process in generating inflammation in the body.
Leukotriene modifiers work through two distinct mechanisms:
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...
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.

You might also read

Related Articles

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

Sort by
Same author

AAVrh.10hFXN Gene Therapy for the Cardiomyopathy of Friedreich Ataxia: A Nonrandomized Clinical Trial.

JAMA cardiology·2026
Same author

Impact of population-specific pharmacogenomic variants on drug dosing in ICU patients.

The pharmacogenomics journal·2026
Same author

Consequences of human genetic variations in <i>KIAA0319L</i>, encoding adeno-associated virus receptor, on AAV-mediated gene transfer.

Molecular therapy. Advances·2026
Same author

Lung microbiome predictors of epigenetic aging and potential associations with smoking and electronic cigarette use.

Clinical epigenetics·2026
Same author

Smoking-induced dysregulation of transposable elements in the small airway epithelium.

Respiratory research·2026
Same author

Prime Editing of Alzheimer's Disease High-Risk APOE4 Allele by Brain-Directed Adeno-Associated Virus Vectors.

Human gene therapy·2025
Same journal

Number Needed to Treat with Biologics in Type-2 Inflammation COPD: A Systematic Review and Meta-Analysis.

COPD·2026
Same journal

Global, Regional, and National Burden of COPD Attributable to Secondhand Smoke from 1990 to 2021: Findings from the Global Burden of Disease Study 2021.

COPD·2026
Same journal

Upregulation of LncRNA MIR31HG in COPD Correlates with Disease Severity and Facilitates Inflammation via miR-342-3p.

COPD·2026
Same journal

Methodological Considerations in the Development of the AECOPD "Infection Score".

COPD·2026
Same journal

Barriers and Facilitators to Treatment Plan Adoption and Self-Management in People with Chronic Obstructive Pulmonary Disease (COPD): A Systematic Search and Narrative Synthesis.

COPD·2026
Same journal

Airway Mucus Occlusions in Ex-Smokers with and Without COPD.

COPD·2026
See all related articles

Related Experiment Video

Updated: May 13, 2026

Bronchial Thermoplasty: A Novel Therapeutic Approach to Severe Asthma
14:39

Bronchial Thermoplasty: A Novel Therapeutic Approach to Severe Asthma

Published on: November 4, 2010

Alpha-1 antitrypsin augmentation therapy.

Mark D Wewers1, Ronald G Crystal

  • 1Davis Heart and Lung Research Institute, Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Internal Medicine, The Ohio State University, Wexner Medical Center, Columbus, Ohio, USA.

COPD
|March 27, 2013
PubMed
Summary
This summary is machine-generated.

Alpha-1 antitrypsin deficiency (AATD) therapy involves intravenous infusions of alpha-1 antitrypsin (AAT) to combat lung damage. This treatment effectively manages the only genetic lung disease with a therapy for all affected individuals.

Related Experiment Videos

Last Updated: May 13, 2026

Bronchial Thermoplasty: A Novel Therapeutic Approach to Severe Asthma
14:39

Bronchial Thermoplasty: A Novel Therapeutic Approach to Severe Asthma

Published on: November 4, 2010

Area of Science:

  • Pulmonary Medicine
  • Genetics
  • Pharmacology

Background:

  • Alpha-1 antitrypsin deficiency (AATD) is a common hereditary disease.
  • AATD results from genetic variations causing deficient liver production of alpha-1 antitrypsin (AAT).
  • AAT inhibits neutrophil elastase (NE), an enzyme that causes emphysema when unchecked.

Purpose of the Study:

  • To describe the development and success of AAT augmentation therapy for AATD.
  • To highlight AATD as a unique genetic pulmonary disease with effective treatment.

Main Methods:

  • Understanding AATD pathophysiology: genetic basis, AAT function, and NE's role in emphysema.
  • Developing intravenous AAT infusions using purified human plasma.
  • Conducting clinical trials to confirm efficacy and safety of weekly AAT infusions.

Main Results:

  • Weekly AAT infusions successfully raised plasma and lung AAT levels to normal in AATD patients.
  • AAT augmentation therapy is now a globally recognized treatment for AATD.
  • This represents a significant medical advancement in treating a common hereditary disease.

Conclusions:

  • AAT augmentation therapy is a triumph over AATD, effectively treating the pulmonary manifestations.
  • It is the only effective therapy available for all individuals with this genetic lung disease.