Lung cells damage caused by inhalation of silica and silicon crystals leads to Silicosis. Retinoic acid is a mitogen in the development of lung organs and exerts pleiotropic effects on immune reactions. How retinoic acid signaling engaged in Silicosis remains unknown. We report here that retinoic acid signaling in dendritic cells was activated in silicosis lesions. SiO2 activates the retinoic acid signaling by provoking ferroptosis. Ferroptosis trigger a downstream “retinoic acid inflammation” characterized by upregulating cGAS-STING signaling genes and inflammasome associated IL-1βand IL-1α. However, knockdown of retinoic acid receptor α slightly mitigates ferroptosis-induced cell death. Inhibition of ferroptosis in mice relieves silica-induced lung inflammation and fibrosis. This cellular retinoic acid response may act as a cytosolic adjuvant to promote extended and upgraded inflammation. Our work unveils a mechanism by which retinoic acid reaction integrates cGAS-STING and inflammasome signaling to sustain silica-induced inflammation.