Lung regeneration and repair machinery and cellular metabolism
In response to environmental injuries, adult lungs will reactivate a series of developmental important
pathways, such as Hedgehog, TGF-beta, Wnt/beta-catenin and Notch pathways to fulfill the
regeneration functions. We are interested to address how COPD GWAS genes regulate
these developmental important pathways in postnatal stage thus modulate the lung
repair/regeneration capacity upon chronic injuries in distal lungs. Functions of these GWAS genes,
possibly triggering or balancing two or more these developmental pathways in lung progenitor cells
will determine the fate of the diseases in response to different types of injuries that vary in type,
duration and intensity.
Bioenergetics homeostasis is important for cells to sustain normal functions and defend against
injury. Genetics controls on bioenergetics homeostasis, including lipid and glucose metabolism
remain poorly understood in chronic obstructive pulmonary diseases (COPD). Our recent data have
suggested that regulation on cellular or even whole body metabolism might be a shared mechanism
among COPD GWAS genes that may potentially determine the cellular injury response and/or repair
capacity in lung epithelial cells in response to chronic cigarette smoke exposure.