Ongoing Research Lines

Extracellular matrix and fibrosis in cardiac adverse and reverse remodeling

We test the role of extracellular matrix proteins, particularly Tenascin C (TNC) in the progression of ischemic heart disease and clarify the maladaptive role of TNC in cardiac fibrosis and inflammation

Cardiac energetics and metabolism in left ventricular hypertrophy and hypertrophic cardiomyopathy

We focus the mechanism of reverse remodeling after the mechanical unloading the heart, e.g. after heart valve replacement, and to address the cardiac fibrosis in myocardial stiffness. In addition, our goal to establish small animal model of hypertrophic cardiomyopathy and test the efficacy of SGLT2i in respect to cardiac metabolism, lipids accumulation and fibrosis.

Novel (non)-pharmacological approaches to treat myocardial ischemia/reperfusion injury

In collaboration with pharmaceutical and biotechnology companies and academic research group, we test novel approaches to mitigate myocardial ischemia and reperfusion-injury in small or large animal models.

The impact of cancer and cancer-cachexia on cardiac metabolism, contractility and inflammation

Treatment of HF in individuals with cancer is the same as for HF in other populations, despite the pathophysiology being different. Antitumor therapies may be cardiotoxic, and solid cancer in and of itself can initiate a specific cardiomyopathy. The evidence regarding this latter has mainly been gathered from mouse models of advanced cancer and has been buttressed by small clinical studies, which highlighted cardiac abnormalities in subjects with solid malignancies. Nevertheless, there is limited knowledge about the prevalence and features of cancer-related cardiomyopathy. Our aim to directly promote or precipitate HF (cancer-induced HF) and can magnify the detrimental effects of traditional risk factors for HF, as well as of cardiotoxic antineoplastic therapies (cancer-enabled HF). Inflammation has been pointed out as a main driver of cancer-related cardiomyopathy arising in the presence of tumours leading to cachexia but may not be equally important when cancer is at an earlier stage. Other mechanisms are likely active and might be therapeutically modulated. Here, we predominantly focus on the role of deranged cardiac metabolism.

Novel approaches to treat cardiac fibrosis, and cardiac dysfunction in Duchenne Muscular Dystrophy

Loss-of-function mutations in gene encoding dystrophin (Dys) results in Duchenne Muscular Dystrophy (DMD). Cardiomyopathy can occur in DMD, and it is also associated with premature senescence of cardiomyocytes, oxidative stress and fibrotic and fat deposition in the ECM. As dystrophin has a role in connecting the muscle cell to the extracellular matrix and this way stabilising the sarcolemma during muscle contraction, its lack results in membrane instability, muscular fibre necrosis, ECM remodeling and compromised muscle regenerating capacity. Consequently, cardiac fibrosis has been detected in DMD patients and the amount of fibrosis predicts the decline of heart function. Here, we aim to better understand the mechanism of the progression of cardiomyopathy in DMD and design novel therapeutic to mitigate the progressive cardiac dysfunction. In collaboration with Prof Oudit (Canada), we also have access to use cardiac MRI data, and address circulating biomarkers for the disease progression in DMD patients.