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The biology of ST2: the International ST2 Consensus Panel.

Publication ,  Journal Article
Pascual-Figal, DA; Januzzi, JL
Published in: Am J Cardiol
April 2, 2015

ST2 is a member of the interleukin 1 receptor family with 2 main isoforms: transmembrane or cellular (ST2L) and soluble or circulating (sST2) forms. ST2 is the receptor of the IL-33, which is an IL-1-like cytokine that can be secreted by living cells in response to cell damage. IL-33 exerts its cellular functions by binding a receptor complex composed of ST2L and IL-1R accessory protein. The IL-33/ST2 system is upregulated in cardiomyocytes and fibroblasts as response to mechanical stimulation or injury. The interaction between IL33 and ST2L has been demonstrated to be cardioprotective: in experimental models, this interaction reduces myocardial fibrosis, prevents cardiomyocyte hypertrophy, reduces apoptosis, and improves myocardial function. The beneficial effects of IL-33 are specifically through the ST2L receptor. sST2 avidly binds IL-33 which results in interruption of the interaction between IL-33/ST2L and consequently eliminates the antiremodeling effects; thus, sST2 is viewed as a decoy receptor. In recent years, knowledge about ST2 role in the pathophysiology of cardiovascular diseases has broadly expanded, with strong links to myocardial dysfunction, fibrosis, and remodeling. Beyond its myocardial role, the IL-33/ST2 system could have an additional role in the development and progression of atherosclerosis. In conclusion, IL-33/ST2L signaling is a mechanically activated, cardioprotective fibroblast-cardiomyocyte paracrine system, which may have therapeutic potential for beneficially regulating the myocardial response to overload and injury. In contrast, sST2 acts as a decoy receptor and, by sequestering IL-33, antagonizes the cardioprotective effects of IL-33/ST2L interaction.

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Published In

Am J Cardiol

DOI

EISSN

1879-1913

Publication Date

April 2, 2015

Volume

115

Issue

7 Suppl

Start / End Page

3B / 7B

Location

United States

Related Subject Headings

  • Receptors, Cell Surface
  • Myocytes, Cardiac
  • Interleukin-1 Receptor-Like 1 Protein
  • Humans
  • Consensus
  • Cardiovascular System & Hematology
  • Cardiovascular Diseases
  • Apoptosis
  • 3201 Cardiovascular medicine and haematology
  • 1102 Cardiorespiratory Medicine and Haematology
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Pascual-Figal, D. A., & Januzzi, J. L. (2015). The biology of ST2: the International ST2 Consensus Panel. Am J Cardiol, 115(7 Suppl), 3B-7B. https://doi.org/10.1016/j.amjcard.2015.01.034
Pascual-Figal, Domingo A., and James L. Januzzi. “The biology of ST2: the International ST2 Consensus Panel.Am J Cardiol 115, no. 7 Suppl (April 2, 2015): 3B-7B. https://doi.org/10.1016/j.amjcard.2015.01.034.
Pascual-Figal DA, Januzzi JL. The biology of ST2: the International ST2 Consensus Panel. Am J Cardiol. 2015 Apr 2;115(7 Suppl):3B-7B.
Pascual-Figal, Domingo A., and James L. Januzzi. “The biology of ST2: the International ST2 Consensus Panel.Am J Cardiol, vol. 115, no. 7 Suppl, Apr. 2015, pp. 3B-7B. Pubmed, doi:10.1016/j.amjcard.2015.01.034.
Pascual-Figal DA, Januzzi JL. The biology of ST2: the International ST2 Consensus Panel. Am J Cardiol. 2015 Apr 2;115(7 Suppl):3B-7B.
Journal cover image

Published In

Am J Cardiol

DOI

EISSN

1879-1913

Publication Date

April 2, 2015

Volume

115

Issue

7 Suppl

Start / End Page

3B / 7B

Location

United States

Related Subject Headings

  • Receptors, Cell Surface
  • Myocytes, Cardiac
  • Interleukin-1 Receptor-Like 1 Protein
  • Humans
  • Consensus
  • Cardiovascular System & Hematology
  • Cardiovascular Diseases
  • Apoptosis
  • 3201 Cardiovascular medicine and haematology
  • 1102 Cardiorespiratory Medicine and Haematology