It is well accepted that epigenetic modification, genetic mutation, and impairment in the spatio-temporal expression may play a critical role in the pathogenesis of lung and heart diseases such as lung fibrosis, pulmonary arterial hypertension, chronic obstructive pulmonary disease, asthma, and heart failure. However, the molecular blueprint is still missing, and the mechanisms linking the molecular profile with enhanced susceptibility, vulnerability, and clinical severity remain largely unknown.

Our research aims to define the molecular signature in lung diseases and understand how it may affect disease development and severity.

We study the intricate interplay of molecular pathways implicated in lung and heart disorders. These pathways function across various tiers: transcriptional, epigenetic, and protein levels. To bridge the divide between our controlled laboratory settings and real-world disease processes, our research group uses a translational methodology. We conduct in-depth in vitro investigations in human cells and leverage animal models of Pulmonary Arterial Hypertension and Pulmonary Fibrosis. This approach enables us to assess and validate the effectiveness of novel experimental treatments, encompassing pharmacological compounds and gene therapy interventions.