Research

In this section, you can find information about our main research lines and the experimental models we use.

Impaired Desmin Homeostasis as a Contributor to Heart Failure Development

Disruption of desmin homeostasis represents a key pathological feature in multiple forms of heart failure. The progressive accumulation of desmin aggregates within cardiac myocytes compromises the highly organized ultrastructure essential for proper contractile function. Beyond structural disintegration, these aggregates exert specific cellular toxicity, triggering molecular pathways that further damage cardiac cells. This dual impact—loss of structural integrity combined with toxic gain of function—plays a critical role in the progression of cardiac dysfunction, highlighting desmin as both a marker and potential therapeutic target in heart disease.

Search and Validation of New Therapies Targeting Prodromic, Toxic, Desmin Proteoforms and their Aggregates to curb Ischemic and Non-Ischemic Heart Disease and HFpEF

Study of the Detailed Mechanisms of Cellular Toxicity for DesminAggregates

Optimization of Targeted Approaches to Measure DesminProteoforms by Mass Spectrometry

Role and Significance of Desmin IF in Phase-Partition in the Heart

  • Primary Cardiomyocyte Cultures from Human Heart Explants
  • iPSC-CM
  • Purified Desmin In Vitro Models (Hydrogels)