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Both exhibit aberrant expression in silica-exposed alveolar macrophages (AMs), thereby altering cellular fate. Given the central role of AMs in silicosis pathogenesis, silica-induced CDK\/CDKI dysregulation likely contributes to the pathogenesis of silicosis. However, the detailed processes have never been systematically described. In this review, we first summarized the origins of AMs and their recruitment to lung tissue following silica exposure. We then introduced the molecular mechanisms by which silica particles induce CDK\/CDKI dysregulation in AMs, including their molecular forms, distribution, degradation, and the signaling pathways involved. Subsequently, we reviewed how CDK\/CDKI dysregulation affects pulmonary fibrosis by reprogramming macrophage fate, encompassing pyroptosis, apoptosis, ferroptosis, and polarization. Finally, we explored the therapeutic potential, current challenges, and future strategies of targeting CDK\/CDKI in silicosis fibrosis. 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