Research

Many skeletal diseases are largely associated with or caused by inflammation. However, the underlying mechanisms are far from understood. Our lab studies osteoimmunology, an interdisciplinary field linking bone biology and the immune system, focusing on inflammatory regulation of gene expression and signaling in macrophage differentiation to osteoclasts (see the
model of a new molecular regulatory network we recently identified), adipogenesis, skeletal damage and repair involved in disease (such as osteoporosis and inflammatory arthritis). We equip genetic approaches (knockout and transgenic mice), primary cells (for example,
bone marrow cells and PBMCs), a combination
of molecular and cellular methods, various
next-generation techniques (RNAseq,
ATACseq, ChIPseq, scRNAseq), multi-omics
approaches, and disease models (such as RA,
osteoporosis, fracture, high fat diet-induced
obesity/type-2 diabetes mouse models). We
work extensively on signal transduction and
crosstalk, genetic and epigenetic regulation of
gene transcription and function, cell
differentiation and in vivo bone remodeling and
metabolism. We are dedicated to advancing
scientific knowledge addressing how the
immune system regulates the skeleton and
identifying novel therapeutic targets for

improving musculoskeletal diseases

associated with inflammation.