ROLE OF SENESCENCE IN CARDIOVASCULAR DISEASES
In vitro model of senescence in human cardiomyocytes: LCT is active in studying the role of senescence in cardiovascular diseases. In particular, an in vitro model of premature senescence in human cardiomyocytes (functional cardiac cells) was developed using the Induced Pluripotent Stem Cells (iPS) technology. This model is a unique platform for the study of cellular mechanisms lying behind senescence-associated cardiac disease in human. The platform will be the basis of an important study aiming to evaluate the susceptibility of senescent cardiomyocytes to SARS-CoV-2.
In-vivo stress-induced senescence: The role of senescence is also studied in-vivo in animal model of myocardial infarction. The acute ischemic event induces the formation of fibrotic tissue and the accumulation of senescent cells that release factors that can alter the functionality of heart cells. This may contribute to exacerbate the necrosis process resulting from the acute ischemic event. We aim to studying possible “senolytic” and/or “senostatic” approaches to ameliorate senescence-associated damage in the heart.
EXOSOMES AND EXTRACELLULAR VESICLES AS LIQUID BIOPSY
EV as Biomarkers. Recently, the LCT laboratory has completed a series of studies performing molecular analysis of the biofluid-derived extracellular vesicles (EV). We profiled surface protein and membrane lipids of plasma and serum-derived EV. The EV-based diagnostic test standardized at LCT laboratory has been evaluated as diagnostic tool in acute cardiac rejection following heart transplantation to discriminate different types of rejection as well as for prognosis of severity of rejection. We recently evaluated the lipid composition of circulating EVs and their diagnostic potential after myocardial ischemia. Very recently we used the profiling of EV as prognostic tool for predicting severity in COVID-19 patients. Role of EV as Mediators of Inflammation. The laboratory has made important advances in research studying the role of circulating EVs resulting from the inflammatory process following an acute ischemic event of the myocardium. We proved that inflammatory EV secreted by polarized macrophages carrying inflammatory cytokine such as IL-1α, IL-1β e have direct cytotoxic effects on heart cells.
