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

Introduction to Fibroblasts01:09

Introduction to Fibroblasts

4.1K
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...
4.1K

You might also read

Related Articles

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

Sort by
Same author

Mesothelial Plasticity Specifies a Pleural Immune Circuit that Orchestrates Lung Regeneration.

bioRxiv : the preprint server for biology·2026
Same author

Sarcoidosis: A Clinical Trials Perspective.

Pulmonary therapy·2026
Same author

Advances in Sarcoidosis.

Archivos de bronconeumologia·2026
Same author

Exploring glucocorticoid receptor signalling in lymphangioleiomyomatosis.

ERJ open research·2026
Same author

Disorders of Telomere Length.

NEJM evidence·2026
Same author

Comparative Transcriptional Profiling of Key Macrophage and Fibroblast Subpopulations in Rheumatoid Arthritis-Associated Lung Disease.

Arthritis & rheumatology (Hoboken, N.J.)·2026

Related Experiment Video

Updated: Feb 23, 2026

Refined Murine Model of Idiopathic Pulmonary Fibrosis
07:51

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Published on: June 17, 2025

1.2K

IPF lung fibroblasts have a senescent phenotype.

Diana Álvarez1,2, Nayra Cárdenes1,2, Jacobo Sellarés1,2

  • 1The Dorothy P. and Richard P. Simmons Center for Interstitial Lung Disease, Pittsburgh, Pennsylvania.

American Journal of Physiology. Lung Cellular and Molecular Physiology
|September 2, 2017
PubMed
Summary

Idiopathic pulmonary fibrosis (IPF) lung cells show increased aging hallmarks, including senescence and a detrimental secretory phenotype. These findings suggest aging fibroblasts, not just aberrant activation, drive IPF progression.

Keywords:
TGF-βagingcollagenfibroblastsidiopathic pulmonary fibrosismitochondriasenescencetelomeres

More Related Videos

Induction and Validation of Cellular Senescence in Primary Human Cells
08:18

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

18.1K
A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
06:35

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth

Published on: December 22, 2020

5.2K

Related Experiment Videos

Last Updated: Feb 23, 2026

Refined Murine Model of Idiopathic Pulmonary Fibrosis
07:51

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Published on: June 17, 2025

1.2K
Induction and Validation of Cellular Senescence in Primary Human Cells
08:18

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

18.1K
A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
06:35

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth

Published on: December 22, 2020

5.2K

Area of Science:

  • Cellular Biology
  • Aging Research
  • Pulmonary Medicine

Background:

  • Idiopathic pulmonary fibrosis (IPF) pathogenesis remains unclear, particularly concerning aging mechanisms.
  • The role of human lung fibroblasts (hLFs) in IPF is recognized, but their behavior in aging lungs is understudied.

Purpose of the Study:

  • To investigate age-related changes in primary hLFs from IPF patients compared to age-matched controls.
  • To determine if cellular senescence and associated phenotypes contribute to IPF development.

Main Methods:

  • Isolation and characterization of primary hLFs from IPF lungs and age-matched controls.
  • Assessment of aging hallmarks: senescence markers (β-galactosidase, p21, p16, p53), proliferation, apoptosis, telomere length, mitochondrial function, and endoplasmic reticulum stress.
  • Evaluation of senescence-associated secretory phenotype (SASP) cytokine expression.

Main Results:

  • IPF hLFs exhibited increased cellular senescence, higher expression of senescence markers, and elevated SASP factors compared to controls.
  • IPF hLFs showed decreased proliferation and apoptosis.
  • Shorter telomeres, mitochondrial dysfunction, and increased endoplasmic reticulum stress were observed in IPF hLFs, particularly after TGF-β stimulation.

Conclusions:

  • IPF hLFs display a distinct senescence phenotype characterized by reduced apoptosis and increased SASP.
  • SASP in IPF hLFs may significantly contribute to the fibrotic process in the aging lung.
  • These findings suggest a paradigm shift from aberrantly activated fibroblasts to senescent cells in IPF pathology.