IL-33 and ST2 comprise a critical biomechanically induced and cardioprotective signaling system.

By S. Sanada, D. Hakuno, Luke J. Higgins, E. Schreiter, Andrew N. J. McKenzie, Richard T. Lee. Journal of Clinical Investigation, 2007

1,045 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/89eaeb88447c8098ce3c6eee4296acfd9466a9db

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

Citations in the corpus

Cardiac fibrosis. (2020, background): “In the pressureoverloaded myocardium, IL-33 was found to exert cardioprotective and anti-fibrotic actions, attributed to its binding to the ST2 receptor in cardiomyocytes and fibroblasts.(177) However, considering the potent effects of the IL-33/ST2 axis on cardiomyocytes, macrophages and lymphocyte”
Disease-associated functions of IL-33: the new kid in the IL-1 family (2010, background): “At the protein level, IL-33 is mainly expressed by fibroblast”
IL‐1, IL‐18, and IL‐33 families of cytokines (2008, background): “In a recent study, IL-33 and T1/ST2 were shown to participate in a paracrine signaling system between cardiac fibroblasts and cardiomyocytes to modulate cardiac hypertrophy and fibrosis (175).”
Anatomy, Function, and Dysfunction of the Right Ventricle: JACC State-of-the-Art Review. (2019, background): “However, trophic paracrine signals from stretched cardiac fibroblasts may be equally important (56).”
THE INTERLEUKIN-1 FAMILY: BACK TO THE FUTURE (2013, neutral): “In cardiovascular diseasemodels, IL-33 plays a protective role by reducing atherosclerotic plaque formation (Miller et al., 2008) or by reducing cardiac hypertrophy secondary to pressure overload (Sanada et al., 2007).”
The interleukin‐1 receptor/Toll‐like receptor superfamily: 10 years of progress (2008, background): “IL-33 is a potent activator of Th2 cells and has been shown to have various other effects, including a protective effect in atherosclerosis as well as a more general cardioprotective effect (26, 27).”
The IL-1-like cytokine IL-33 is inactivated after maturation by caspase-1 (2009, background): “Based on animal model studies and analyses of diseased tissues from patients, IL-33 has been proposed to represent a promising therapeutic target for several important diseases, including asthma and other allergic diseases (4), rheumatoid arthritis (5, 6), atherosclerosis (7), and cardiovascular dis”
The IL-33/ST2 pathway: therapeutic target and novel biomarker (2008, background): “As will be discussed in this Review, myocardial production of IL-33 can protect cardiac function in response to pressure overloa”