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Targeting this pathway represents a promising strategy to prevent liver IR injury; however, existing CD47 antagonists cause severe hematologic side effects due to nonspecific binding to erythrocytes. This study developed TAX2 (CD47\u2010derived peptide with the sequence CEVSQLLKGDAC)\u2010functionalized biodegradable nanoparticles (TAX2\u2010NPs) that specifically capture TSP\u20101 and block its interaction with CD47 on liver sinusoidal endothelial cells (LSECs). TAX2\u2010NPs are composed of PLGA and DSPE\u2010PEG\u2010Mal and are conjugated with the cyclic peptide TAX2, derived from the TSP\u20101\u2010binding domain of CD47. Upon systemic administration, TAX2\u2010NPs preferentially accumulate in the injured liver, where they competitively bind TSP\u20101, preventing endothelial apoptosis and preserving sinusoidal integrity. Captured TSP\u20101 is subsequently internalized by macrophages and degraded via the autophagy\u2010lysosome pathway, thereby eliminating residual extracellular TSP\u20101 and mitigating its prolonged pathogenic effects. 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