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Related Concept Videos

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.
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...
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:
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Introduction to Fibroblasts01:09

Introduction to Fibroblasts

Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...
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Cystic Fibrosis: Pathogenesis

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Related Experiment Video

Updated: May 22, 2026

Refined Murine Model of Idiopathic Pulmonary Fibrosis
07:51

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Published on: June 17, 2025

Cellular players in lung fibrosis.

Annemarie N Lekkerkerker1, Jamil Aarbiou, Thomas van Es

  • 1Galapagos BV, AC Leiden, The Netherlands.

Current Pharmaceutical Design
|May 29, 2012
PubMed
Summary

Fibrosis involves myofibroblasts originating from various sources, including resident fibroblasts, epithelial cells via epithelial to mesenchymal transition (EMT), and bone marrow-derived fibrocytes. Understanding these fibrotic cells is key for drug discovery.

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Area of Science:

  • Cell Biology
  • Pathology
  • Pulmonology

Background:

  • Fibrosis, a common feature in various organ diseases, is characterized by excessive extracellular matrix deposition.
  • Myofibroblasts are key effector cells in fibrosis, with their origins being a significant area of research.

Purpose of the Study:

  • To review the potential origins and roles of fibrotic cells in lung fibrosis.
  • To discuss in vitro models for studying these cells and their therapeutic potential.

Main Methods:

  • Literature review of studies on fibrotic cell origins and mechanisms.
  • Discussion of in vitro models for studying fibrotic cells.

Main Results:

  • Myofibroblasts in lung fibrosis may originate from resident fibroblasts, epithelial-mesenchymal transition (EMT), and fibrocytes.
  • Alternatively activated macrophages and TGF-beta play crucial roles in promoting fibrosis.

Conclusions:

  • Multiple cell types contribute to myofibroblast accumulation in lung fibrosis.
  • In vitro models provide avenues for identifying novel therapeutic targets for fibrotic diseases.