RESEARCH ACTIVITY

Cardiovascular (heart and vessel) disaeases are the leading cause of morbidity and mortality worldwide. Intriguingly, the cardiovascular system has the intrinsic potential to protect itself against damage induced by ischemia/reperfusion and cardiotoxic substances.

In the Cardiovascular Physiology laboratories, research is carried out to clarify the mechanisms of cardiovascular protection against damage induced directly or indirectly by various factors [ischemia / reperfusion (I / R), chemical (Herbicides and derivatives)] and the endogenous repair potential of the myocardial injury in terms of endogenous molecules (e.g. apelin, gas transmitters Hydrogen sulphide) and potentially therapeutic protective protocols (e.g. remote conditioning). Cardioprotection by remote conditioning is induced with brief ischemia of the limbs.

Ischemia / reperfusion (I / R) damage repair project. The mechanisms of cardioprotection are studied through different experimental protocols (in vitro, ex vivo and in vivo murine models) in the presence of two or more diseases or medical conditions (co-morbidities) and compared with those present in healthy conditions (donor heart).  We aim to verify the molecular mechanisms that are the basis of the protective response induced by therapeutic experimental protocols (for example remote conditioning), endogenous biomaterials (e.g. platelets and extracellular vesicles) and exogenous nanomaterials (e.g. oxygen-charged nanocarriers).

Herbicides and derivatives project: Biological effects of sub-toxic levels of herbicides and derivatives on endothelial cells and cardiomyocytes. Role of mitochondria in the deleterious outcome of glyphosate and AMPA exposure.

Apelin-13 projects: Beside cardioprotective effect (inotropic positive effect and limitation of infarct size), the endogenous peptide Apelin-13 also displayed antiarrhythmic action. Altered Connexin-43 (cx-43) expression and distribution in the cardiac tissue has been observed in several cardiac diseases (such as myocardial infarction and diabetes) and this alteration is related to increased incidence of cardiac arrhythmias that can lead to sudden death; we aim to investigate: 1) the role of Apelina-13 in the regulation of cx-43 expression; 2) the molecular mechanism and the role of autophagic process in the regulation of cx-43 expression. In vitro experimental models for the morphological and functional study of cx-43 in both normoxic and hypoxic conditions.