Background and Purpose
Pulmonary fibrosis (PF) is an irreversible lung disease with little efficient treatments. Epithelial-mesenchymal transition (EMT) in alveolar type II (AT II) cells is an initial process for PF in response to multiple insults. We previously identified paraquat (PQ), inducing acute lung injury and PF, as an agonist for STIM1, promoting STIM1-TRPC1 association for intracellular calcium burden and thus EMT. Here, we investigated the strategy targeting STIM1-TRPC1 association and excessive calcium influx in treating PF.