ST2/IL-33 signaling in cardiac fibrosis

Elena Vianello, Elena Dozio, Lorenza Tacchini, Luigi Frati, Massimiliano Marco Corsi Romanelli

Research output: Contribution to journalArticlepeer-review


Cardiac fibrosis is a significant global health problem associated with nearly all forms of heart disease. In the heart interstitial fibrosis may be reparative, replacing areas damaged by myocyte loss after acute infarction, or compensative, responding to cardiac overload. However, after injury in chronic cases activated myofibroblasts contribute to the tissue imbalance of the newer molecules associated with cardiac fibrosis, interleukin (IL-33), and suppression of tumorigenicity 2 (ST2). Physiological stretching causes myofibroblasts to release IL-33 which binds the ST2 receptor (ST2L) on the cardiomyocyte membrane, promoting cell survival and integrity. But in chronic conditions, local and neighboring cells can increase the release of IL-33's decoy, soluble ST2 (sST2), which blocks IL-33/ST2L binding, promoting tissue fibrosis. We review recent studies that have illustrated novel aspects of ST2/IL-33 signaling mediating cardiac fibrosis, and some newer biomolecular targets for the prevention and treatment of maladaptive remodeling.

Original languageEnglish
Pages (from-to)105619
JournalInternational Journal of Biochemistry and Cell Biology
Publication statusPublished - Nov 2019


Dive into the research topics of 'ST2/IL-33 signaling in cardiac fibrosis'. Together they form a unique fingerprint.

Cite this