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.
|Journal||International Journal of Biochemistry and Cell Biology|
|Publication status||Published - Nov 2019|