The research is mainly moving in a couple of directions. 1. Slow down the excessive inflammation and progressive tissue damage by developing targeted therapies against new pro-catabolic molecules.
2. Stimulate the endogenous repair process through biological treatments towards enhancing the activity of resident progenitor cells. The challenge is to identify a single molecule or a combination of molecules with adequate characteristics for satisfying both needs. We are studying the molecular circuits and interactions involving pro-chondrogenic or pro-osteogenic transcription factors (SOX9, TRPS1, RUNX2), the longevity transcription factor FOXO3a, and the microRNA-221; the nucleotide signaling mediated by the P2X7 purinergic receptor (P2X7R), commonly involved in the origination and maintenance of inflammatory pathways mediating catabolic cascade through the release of cytokines.
