TRPC3 and bronchopulmonary dysplasia: Therefore, we hypothesized that in a neonatal hyperoxic lung injury rat model of BPD, the simplification of alveoli and pulmonary blood vessels would reduce the expression of TRPC3 in the lungs, and the decreased TRPC3 expression would impair cell membrane permeability and inhibit cell proliferation, thereby promoting the development of BPD and participating in the regulation of BPD through the nuclear factor‐κB (NF‐κB) signaling pathway.