Related Experiment Video

Updated: Jan 29, 2026

Adoptive Transfer of IL-33-Stimulated Macrophages into Bleomycin-Induced Mouse Models to Study Their Effect on Idiopathic Pulmonary Fibrosis In Vivo
06:29

Adoptive Transfer of IL-33-Stimulated Macrophages into Bleomycin-Induced Mouse Models to Study Their Effect on Idiopathic Pulmonary Fibrosis In Vivo

Published on: May 5, 2023

3.1K

Dysregulation of IL-33/ST2 signaling and myocardial periarteriolar fibrosis

Jessica C Garbern1, Jason Williams2, Amy C Kristl3

  • 1Department of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, 7 Divinity Ave, Cambridge, MA 02138, United States of America; Department of Cardiology, Boston Children's Hospital, 300 Longwood Ave, Boston, MA 02115, United States of America.

Journal of Molecular and Cellular Cardiology
|February 15, 2019
PubMed

Insights

Interleukin-33 (IL-33) receptor ST2 signaling loss, not IL-33 levels, may drive periarteriolar fibrosis in aging and pressure overload. This pathway manipulation may not fully prevent or reverse cardiac fibrosis.

Area of Science:

  • Cardiovascular biology
  • Fibrosis research
  • Molecular mechanisms of heart disease

Background:

  • Diastolic dysfunction in heart failure with preserved ejection fraction is linked to cardiac microvascular dysfunction and periarteriolar fibrosis.
  • Interleukin-33 (IL-33), acting through its receptor ST2, is known to prevent global myocardial fibrosis under pressure overload.
  • The specific role of the IL-33/ST2 pathway in regulating periarteriolar fibrosis remains largely undetermined.

Purpose of the Study:

  • To investigate the role of the IL-33/ST2 axis in modulating periarteriolar fibrosis.
  • To examine age-related changes in IL-33 and ST2 expression and their correlation with periarteriolar fibrosis.
  • To determine the impact of IL-33 or ST2 deficiency on periarteriolar fibrosis following pressure overload.

Main Methods:

  • Comparative analysis of IL-33 and ST2 expression in young versus aged wild-type mice.
  • Induction of pressure overload via transverse aortic constriction (TAC) in mice genetically deficient in IL-33 or ST2.
  • Histological assessment of periarteriolar fibrosis in aged and TAC-subjected mice.

Main Results:

  • Aging was associated with increased IL-33 expression, decreased ST2 expression, and enhanced periarteriolar fibrosis.
  • Mice lacking ST2 exhibited significantly increased periarteriolar fibrosis after TAC compared to wild-type controls.
  • Mice deficient in IL-33 did not show a significant increase in periarteriolar fibrosis post-TAC.

Conclusions:

  • Loss of ST2 signaling, rather than altered IL-33 expression, appears to be a key factor in the development of periarteriolar fibrosis during aging and pressure overload.
  • While the IL-33/ST2 pathway is implicated, targeting it alone may not be sufficient to prevent or reverse cardiac fibrosis.

Keywords:
AgingInterleukin-33Myocardial fibrosisPeriarteriolar fibrosisPressure overloadST2

More Related Videos

Ultrasonic Assessment of Myocardial Microstructure10:53

Ultrasonic Assessment of Myocardial Microstructure

Published on: January 14, 2014

5.8K
Myocardial Infarction and Functional Outcome Assessment in Pigs12:03

Myocardial Infarction and Functional Outcome Assessment in Pigs

Published on: April 25, 2014

28.7K

Related Concept Videos

Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
868
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...
520
Endocrine Signaling01:45

Endocrine Signaling

Endocrine cells produce hormones to communicate with remote target cells found in other organs. The hormone reaches these distant areas using the circulatory system. This exposes the whole organism to the hormone but only those cells expressing hormone receptors or target cells are affected. Thus, endocrine signaling induces slow responses from its target cells but these effects also last longer.
68.1K
Bacterial Signaling01:30

Bacterial Signaling

Bacterial signaling can occur within bacteria (intracellular) or between bacteria (intercellular). At times, a group of bacteria behaves like a community. To achieve this, they engage in quorum sensing, the perception of higher cell density that causes changes in gene expression. Quorum sensing involves both extracellular and intracellular signaling. The signaling cascade starts with a molecule called an autoinducer (AI). Individual bacteria produce AIs that move out of the bacterial cell...
40.6K
Yeast Signaling01:28

Yeast Signaling

Yeasts are single-celled organisms, but unlike bacteria, they are eukaryotes (cells with a nucleus). Cell signaling in yeast is similar to signaling in other eukaryotic cells. A ligand, such as a protein or a small molecule released from a yeast cell, attaches to a receptor on the cell surface. The binding stimulates second-messenger kinases to activate or inactivate transcription factors that further regulate gene expression. Many of the yeast intracellular signaling cascades have similar...
17.2K
What is Cell Signaling?02:03

What is Cell Signaling?

Despite the protective membrane that separates a cell from the environment, cells need the ability to detect and respond to environmental changes. Additionally, cells often need to communicate with one another. Unicellular and multicellular organisms use a variety of cell signaling mechanisms to communicate to respond to the environment.
130.3K