Corneal Wound Healing and Neovascularization
Qing Lin, MD, PhD

Injury to the cornea, such as from chemical burns or transplantation, can trigger corneal neovascularization. The ingrowth of abnormal blood vessels into the normally transparent cornea threatens vision and can result in blindness. Dr. Lin’s work has demonstrated that corneal injury activates damage-associated molecular pattern (DAMP) signaling. In particular, the DAMP molecule HMGB1, acting as a pro-angiogenic factor through its receptor TLR4, functions as a critical link between injury, inflammation, and pathologic vascularization.
The Lin laboratory also investigates G protein–coupled receptor (GPCR) pathways in immune regulation. Using gene-modified animal models, human cells, and ex vivo human tissue systems, his team has found that GPCR signaling governs the behavior of mast cells, neutrophils, and macrophages during wound healing. These studies will help define how immune cells control the transition from inflammation to proliferation, thereby shaping angiogenesis and vascular remodeling in the injured cornea and other tissues.
Translationally, Dr. Lin seeks to develop immunotherapies that target DAMP and GPCR pathways to improve corneal wound healing and prevent ocular angiogenesis. His research also extends to wound repair in the lung and skin, which share epithelial barrier features with the cornea. His recent work focuses on achieving regeneration in adult injured tissues by replicating a fetal-like, pre-resolving, immune-tolerant environment using biologics derived from human birth tissues. This pro-regenerative strategy holds promise not only for restoring vision in patients with severe corneal and retinal injuries but also for advancing therapies for fibrotic and vascular diseases across multiple organs.