Qinghua Lin

From single-pathway cascade to network pathophysiology: how genetically engineered mouse models reshaped our understanding of pancreatitis

Evidence is synthesized from genetically engineered mouse models that enhanced trypsinogen autoactivation alone is sufficient for spontaneous disease, that NF-κB-driven inflammation can be initiated independently of trypsin, and that loss of autophagy alone disrupts acinar homeostasis, which reframe pancreatitis as a network pathophysiology with two coupled layers.