Macrophage dysfunction is a key factor in uncontrolled inflammation and tissue injury in sepsis-induced acute lung injury. Metabolic reprogramming serves as a critical bridge linking the septic microenvironment to macrophage dysfunction. During sepsis-induced acute lung injury， macrophages undergo significant reprogramming in glucose metabolism， lipid metabolism， amino acid metabolism， and mitochondrial function. These metabolic alterations drive hyperactivation of pro-inflammatory responses while suppressing anti-inflammatory and tissue-repair functions， ultimately exacerbating lung injury. Therapeutic strategies targeting metabolic reprogramming may be beneficial for anti-inflammatory and tissue-protection， but face challenges of macrophage heterogeneity， metabolic network complexity， and clinical translation barriers. Future research requires in-depth analysis of metabolic signatures across distinct macrophage subsets， development of precise interventions， and exploration of metabolic reprogramming as a prognostic biomarker. This approach may facilitate the emergence of targeted metabolic reprogramming as a novel pathway to improve outcomes in sepsis-induced acute lung injury.