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Chronic granulomatous disease: the European experience

Additionally, advancements in mitochondrial genome editing technology offer hope for the precise manipulation of mitochondrial function and addressing genetic abnormalities in neuroinflammatory diseases

J Hazard Mater 417:126055

Inhibitor of apoptosis-stimulating protein of p53 and isoliquiritin also suppress ferroptosis by attenuating aberrant Fe 2+ accumulation in lung tissue[89, 90]

HO-1, an intracellular enzyme implicated in anti-ferroptotic mechanisms, ameliorates fibrosis by inhibiting the expansion and stimulation of HSCs upon induction with magnesium isoglycyrrhizinate [227] (Fig

doi: 10.1056/NEJM198904063201407