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Such transition was shown to be controlled by the Nuclear Receptor Subfamily 4 Group A Member 1 (Nr4a1), which crucially modulates both the early Ly-6C high monocyte inflammatory and the later Ly-6C low macrophage reparative phases in the infarcted myocardium (172)

Targeting lysosomal function-e.g., via lysosomal stabilizers or ferritinophagy inhibitors-may mitigate ferroptosis in COPD (16)

once daily for 20 days) causes a significant retardation of tumor growth and prolongs the survival of A431 tumor-bearing mice [3]