Corneal biomechanical cues mediated by PAI-2：the origin of PM2.5-induced corneal disease

ABSTRACT: Biomechanical signature is directly correlated with the progression of disease in multiple soft tissues. However, their variations and roles particularly during the disease initiation period remain unclear. Here we report that PM2.5 exposure induces corneal biomechanical cues alterations prior to corneal injury, as evidenced by increased corneal hysteresis in humans, thickened corneal thickness in rats, and enhanced tensile stress and cortical stiffness in HCECs. Specifically, intracellular PAI-2 is identified as a crucial mediator of the biomechanical responses in HCECs. It modulates PM2.5-induced autophagy and inflammation through a PAI-2/myosin II/F-actin/YAP positive feedback loop, which ultimately drives HCEC injury. Furthermore, extracellular secretory PAI-2 levels in tears reflect P

SUBMITTER: Shengjie Hao 

PROVIDER: S-SCDT-10_1038-S44321-025-00341-0 | biostudies-other |

REPOSITORIES: biostudies-other