Pentraxin 3 (PTX3) is an acute-phase protein that was recently demonstrated to play pleiotropic activities in cardiovascular (CV) diseases. Tumor necrosis factor and interleukins up-regulates PTX3 transcription in different cell types (i.e. endothelial cells, phagocytes, smooth muscle cells, fibroblasts and glial cells) involved in atherogenesis. By interacting with numerous ligands, PTX3 acts as a modulatory molecule of complement system, inflammatory response, angiogenesis, and vascular/tissue remodeling. Experimental data point to a beneficial role of PTX3 in atherosclerotic plaque development and vulnerability. Animal studies indicated a protective role of PTX3 signaling in ischemic/reperfusion injury and failing heart. Clinical studies have so far provided contrasting results, highlighting a debated role of PTX3 as an active mediator of endothelial dysfunction, atherosclerotic plaque vulnerability and worse outcome after ischemic events. Therefore, substantial evidence suggests a dual role of PTX3 as modulator or amplifiers of the innate immune response. The final result of PTX3 activation might be determined by a fine tuning of time, space and environmental signals. The aim of this review is to provide an overview of biological properties of PTX3 in CV diseases and to discuss the ability of PTX3 to act as a crossroad between pro- and anti-inflammatory pathways.
Keywords: Atherosclerosis; Cardiovascular diseases; Ischemic stroke; Myocardial infarction; Pentraxin 3.
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