Our group aims to understand the cellular and molecular mechanisms regulating striated muscle regeneration and growth in physiology and pathology, as well as in aging.
The group has made important contributions to regenerative medicine by deciphering signaling pathways controlling skeletal muscle stem cell functions during adult muscle regeneration and growth (Suelves et al, EMBO J, 2004; Lluis et al, EMBO J 2005; Perdiguero et al, EMBO J, 2007; Serrano et al, Cell Metabol 2008). Recently, we uncovered why muscle stem cells lose their homeostatic and regenerative functions with aging, providing new insights for rejuvenation of old muscle. (Sousa-Victor et al, Nature 2014; García-Prat et al. Nature 2016). The group has also pioneered studies demonstrating the relevance of inflammation in muscle regeneration and dystrophy progression, which showed that transplantation of bone marrow from wild type mice could rescue the defective regeneration of mice with inflammatory deficits. The group also demonstrated novel inflammation-driven fibrosis mechanisms, which exacerbate muscular dystrophy severity, and more importantly, that interference with these pathways could prevent (and reverse) fibrosis and disease progression (Suelves et al, J. Cell Biol 2007, Vidal et al, Genes and Dev. 2008; Ardite et al, J. Cell Biol, 2012).
Presently, we want to understand striated muscle regenerative decline in aging and dystrophy by:
- Identifying drivers of muscle stem cell senescence that impair regeneration with aging.
- Identifying drivers of the inflammation-fibrosis axis in aging and dystrophic striated muscles.
- Identifying common pathways between skeletal and cardiac muscles leading to dysfunction in aging and disease.