1.

Skeletal muscle homeostasis. We seek to understand the fundamental mechanisms governing skeletal muscle protein homeostasis, with a focus on the balance between protein synthesis and degradation. We have characterized how proteasome dysfunction impairs muscle growth by disrupting ribosomal biogenesis (Am. J. Physiol.-Cell Physiol., 2021), and discovered an evolutionarily conserved circadian rhythm of myostatin expression across species (J. Cachexia, Sarcopenia and Muscle, 2025). These efforts are supported by a National Natural Science Foundation of China (NSFC) Young Scientists Fund and a Dongguan High-level Hospital Construction Project.

2.

Bone homeostasis. We seek to understand the molecular mechanisms that maintain skeletal integrity. We discovered that ANGPTL4, secreted from brown adipose tissue, acts as a leptin-receptor ligand to regulate chondrogenesis and heterotopic ossification (Proc. Natl. Acad. Sci. USA, 2024), revealing an adipose–bone communication mechanism that contributes to pathological bone formation.

3.

Organ–organ crosstalk in the bone–skeletal muscle axis. We seek to understand how bone and skeletal muscle participate in systemic organ–organ communication. We demonstrated that osteocyte/osteoblast-derived SAA3 mediates bone–liver communication to regulate hepatic cholesterol metabolism (Advanced Science, 2024). An ongoing NSFC General Program (2026–2029) investigates how the bone-derived orphan receptor GPR153 coordinates muscle and adipose tissue homeostasis.