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Within the cyst(e)ine/GSH/GPX4 axis, cysteine is the rate-limiting metabolite for GSH biosynthesis, hence the ferroptosis-inducing activity of cyst(e)ine depletion has largely been attributed to the lowering of intracellular GSH levels and subsequent decrease of GPX4 activity

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Similarly, in SLE patients, depletion of Faecalibacterium species resulted in diminished butyrate production, attenuating its anti-inflammatory properties and thereby exacerbating both disease progression and inflammatory responses [44]