Our aim is to better understand the molecular and cellular mechanisms controlling activation of fibroblasts and to unravel how skin homeostasis depends on fibroblast communication with the surrounding ECM.
Our group aims at investigating the mechanisms underlying the control of connective synthesis and the role of cell-matrix interactions. Fibroblasts represent a heterogeneous group of cells that derive from different cellular origins and they are the key cells orchestrating the formation of connective tissues following any type of injury. Their phenotype and function are regulated by interactions with the surrounding extracellular matrix (ECM), mediated by specific receptors and by the activity of growth factors and cytokines through complex paracrine and autocrine regulatory loops.
We have identified the key role of TGFβ and force transduction for ECM production, elucidated the unusual secretion mode of TGFβ from fibroblasts and macrophages, and delineated unique and overlapping roles of extracellular matrix receptors in wound repair and fibrosis. As a model we use fibroblasts obtained from patients with scleroderma, an autoimmune-driven chronic fibrotic disease that involves the skin but can also affect many other organs. We characterize fibroblast subpopulations, find markers and identify them in their spatial context. Together with V. Malhotra (CRG Barcelona) we collaborate on deciphering mechanisms that control the secretion of collagens and devised options to inhibit secretion and thereby to modulate fibrosis.
We characterize fibroblast subpopulations and identify them in their spatial context. Our in vitro findings together with mouse models aim to better understand the molecular basis of diseases associated with excessive fibroblast activation and to design targeted therapies.
Our aim is to better understand the molecular and cellular mechanisms controlling activation of fibroblasts and to unravel how skin homeostasis depends on fibroblast communication with the surrounding ECM. Our in vitro findings together with mouse models are expected to lead to a better understanding of the molecular basis of diseases associated with excessive fibroblast activation and to design targeted therapies.