Role of new receptors of the innate immune system in cardiovascular diseases

We offer an exciting project in a young and dynamic group with a very nice lab enviroment. Atrial myopathy associated with heart failure (HF) is a consequence of structural, neurohormonal, genetic, electric and functional impairment and, in many cases, is closely linked to left ventricle dysfunction. Recent clinical trial data implicate inflammation as a key player in atrial HF-damage. An increase in the inflammatory response is mainly the result of sustained activation of the innate immune system, and several receptors of the innate immune system are increasingly recognized as new players in the progression of several cardiovascular diseases, including HF.  This “translational project” aims to determine whether new receptors of the innate immune system and its associated signaling pathway have a role in atrial HF-remodeling. We will investigate whether genetic, structural, neurohormonal, electric and functional atrial HF-remodeling is associated with the activation of the receptors of innate immune system in humans and also in large (swine) and small (mice) experimental models of atrial failure. Specific knock-out mice will be utilized to examine whether genetic deletion of the receptors of the innate immune system impairs the progression of atrial HF-myopathy. We also will employ specific cell lines to determine the observed effects. The present study will open an innovative field of research related to new potential pro-inflammatory targets for counteracting atrial myopathy-associated HF. This is a ambitious  and multidisciplinar study that will employ biochemical, imaging, functional and molecular approaches applied to human, large and small experimental models.