Sólveig Thorsteinsdóttir é professora associada no Departamento de Biologia Animal da Faculdade de Ciências da Universidade de Lisboa. Os seus interesses científicos situam-se na área da Biologia do Desenvolvimento. Fez a licenciatura em Biologia na Universidade do Kansas nos EUA em 1985. Obteve o doutoramento em Biologia do Desenvolvimento na Universidade de Utrecht na Holanda em 1995 e realizou um pós-doutoramento na Universidade de Otago na Nova Zelândia em 1996-97. Foi investigadora visitante na Universidade de Brasília em Brasil em 2003-04 e na Universidade de Montpellier em França de 2011-12. Foi presidente da Sociedade Portuguesa de Biologia do Desenvolvimento (www.spbd.pt) em 2014-15 e vice-presidente em 2013-12. É membro da Comissão de Coordenação do Mestrado em Biologia Evolutiva e da Licenciatura em Biologia. É autora ou co-autora de 42 publicações científicas.

I work in Developmental Biology and my research interests center on contributing toward understanding the molecular pathways downstream of the extracellular matrix and how they contribute to development, homeostasis and disease. My group is mostly focused on using our knowledge of skeletal muscle development to unveil the molecular mechanisms downstream of a faulty extracellular matrix, as in muscular dystrophies, and identify pathways of therapeutic potential. In recent years, we have focused our studies on LAMA2 congenital muscular dystrophy (CMD) and have discovered that the disease starts as a myogenesis defect during fetal development in a mouse model for the disease. More specifically, this myogenesis defect involves impaired proliferation and differentiation of muscle cells leading to impaired muscle growth. We have defined three main lines of research: 1. Identify the pathways downstream of laminin 211 that are altered at the onset of LAMA2-congenital muscular dystrophy (CMD) in a mouse model of the disease; 2. Use existing and establishing new mouse and human culture systems to mimic LAMA2-CMD in vitro; 3. Use in vitro approaches to inhibit or activate pathways identified as altered in the mouse model of LAMA2-CMD and assess their effect on reverting the proliferation and myogenic differentiation defects. Our research contributes to basic science and to the understanding of the mechanisms by which mutations in an extracellular matrix molecule initiates disease. Our contribution to applied science consists of identifying druggable targets that can ameliorate disease symptoms in our model systems and, in the future, may contribute to therapy development in humans.