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Dr. Carla Rothlin is Dorys McConnell Duberg Professor of Immunobiology and Professor of Pharmacology at the Yale School of Medicine, and co-leader of the Cancer Immunology Programme at Yale Cancer Centre. She studied biochemistry and pharmacology at the University of Buenos Aires, where she also undertook her postgraduate research under the direction of Dr. Ana Belén Elgoyhen, focussing on nicotinic receptors expressed in the inner ear. Later, she completed her doctorate and moved to San Diego to join Dr. Greg Lemke’s laboratory at the Salk Institute for Biological Studies. In 2009, Dr. Rothlin was named Assistant Professor in Immunobiology at Yale Medical School

The findings, published in the journal Circulation Research, not only highlight the gene regulatory mechanisms that control valve formation, but also offer clues for future medical advances

Neuregulin-1 (Nrg1) plays an essential role in the transformation of the heart from its delicate primordial structure into the powerful beating mature organ 

Dr Sancho heads the CNIC Immunobiology Laboratory, whose work focuses on research into the function of dendritic cells and macrophages, as key immune cells that modulate immunity and inflammation, and the use of these cells in immunotherapy in a wide range of diseases

A multicenter study published in JAMA Cardiology and co-led by scientists at Hadassah Medical Center, Sheba Medical Center, and the CNIC could help in the design of future pharmacological treatments for bicuspid aortic valve

The team led by Dr. Pablo García-Pavía, based at the CNIC and Hospital Puerta de Hierro, has published the first study of a drug able to remove amyloid deposits from the heart

A study published in Nature Cell Biology confirms that caveolae are essential for the mechanical responses of tissues subject to large mechanical forces (such as muscle, heart, blood vessels, and fat), whereas larger membrane depressions (termed 'dolines') are important for the response to weak or medium-strength forces

A CNIC study reveals that mutations previously identified in the gene MINDBOMB1 (MIB1) as causing non-compaction cardiomyopathy either provoke this disease or valve defects, depending on their combination with mutations in modifier genes