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In the ACL, oxidative stress can impair fibroblast function and promote ECM degradation

Molecular biology and pharmacological studies ruled out apoptosis and necroptosis, while increased lipid peroxidation and surface expression of the transferrin receptor implicated ferroptosis as the mechanism of the H 2 O 2 -induced cell death: this was supported by suppression of H 2 O 2 -cytotoxicity by liproxstatin-1, a pharmacological inhibitor of ferroptosis

Complete immobilization produces weak, disorganized repair tissue while progressive loading promotes strong, aligned structures