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Related Concept Videos

Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

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
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.
COPD: Pathogenesis and Clinical Features01:20

COPD: Pathogenesis and Clinical Features

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...
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features01:24

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

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...
Atelectasis II: Pathophysiology01:10

Atelectasis II: Pathophysiology

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 collapsed...
Chronic Obstructive Pulmonary Disease I: Introduction01:23

Chronic Obstructive Pulmonary Disease I: Introduction

Chronic obstructive pulmonary disease is a common, preventable, and treatable respiratory disorder characterized by persistent symptoms and progressive airflow limitation. This limitation results from a combination of small-airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema), both driven by chronic inflammation from exposure to harmful particles or gases.The disease includes two main pathological entities: emphysema, marked by destruction of alveolar walls and...

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[Statistic analysis of some risk factors in breast cancer].

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Related Experiment Video

Updated: Jun 15, 2026

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
14:48

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

Adipokines involvement in lung function.

B Gurzu1, F E Zugun, M Costuleanu

  • 1School of Medicine, Department of Physiology, "Gr.T. Popa" University of Medicine and Pharmacy Iaşi.

Revista Medico-Chirurgicala a Societatii De Medici Si Naturalisti Din Iasi
|March 6, 2010
PubMed
Summary
This summary is machine-generated.

White adipose tissue secretes adipokines, hormones that may link obesity and lung disease. This study reviews adipokine roles in pulmonary function, focusing on key hormones like leptin and adiponectin.

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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

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Last Updated: Jun 15, 2026

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
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Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Area of Science:

  • Endocrinology
  • Pulmonology
  • Obesity Research

Background:

  • White adipose tissue is increasingly recognized as an endocrine organ.
  • Adipokines, hormones secreted by adipose tissue, are implicated in various physiological and pathological processes.
  • Obesity is a known risk factor for several lung diseases, suggesting a potential mediating role for adipokines.

Purpose of the Study:

  • To review the current data on the involvement of adipokines in pulmonary function.
  • To highlight the specific roles of key adipokines, including leptin, adiponectin, and others, in the context of lung health and disease.

Main Methods:

  • Literature review of studies investigating adipokines and lung function.
  • Analysis of data linking specific adipokines to respiratory parameters.
  • Focus on established and emerging adipokines such as leptin, adiponectin, TNF-alpha, VEGF, resistin, HGF, IL-6, angiotensinogen, and apelin.

Main Results:

  • Adipokines demonstrate significant influence on various aspects of pulmonary function.
  • Specific adipokines like leptin and adiponectin have well-documented roles, while others like apelin are emerging areas of research.
  • The collective data suggests a complex interplay between adipose tissue hormones and lung physiology.

Conclusions:

  • Adipokines represent a crucial link between obesity and lung pathophysiology.
  • Understanding adipokine-mediated mechanisms is vital for developing novel therapeutic strategies for obesity-related lung diseases.
  • Further research into the diverse roles of adipokines in pulmonary health is warranted.