SOHLH2 and pulmonary fibrosis: Using AECII specific Sohlh2 CKI mouse model, we confirmed that Sohlh2 overexpression caused mitochondrial damage in AECIIs and spontaneous lung fibrosis, and Sohlh2 in AECIIs also largely enhanced HFD-driven oxidative stress, fibrotic remodeling, inflammation, and cell death.