Power analysis was performed for the in vivo studies. All data were included in the final analysis, and outliers were not excluded. Primary endpoints were prospectively determined, and appropriate corrections were made for multiple testing. Mouse studies were repeated twice. Randomization occurred manually. The human studies were performed once. The objectives of our study were to determine the mechanism through which NTN1 drives pulmonary fibrosis and to test the prespecified hypothesis that its role involves adrenergic nerve remodeling. The units of investigation included genetically modified and WT mice, existing data sets, and archived samples and data from healthy control and IPF participants. The overall design involved evaluation of fibrosis in genetically modified mice or in WT animals subjected to chemical denervation or α1 blocker treatment. Archived samples and historical data from humans were used to support the clinical relevance of our experimental observations. Analysis was performed in triplicate using randomization to avoid block effect. Mice and samples were numerically coded, and animal handlers and laboratory staff were blinded to the study group.

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