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Because of these properties, isolated BPC-157 is of great interest to researchers
provided evidence of B cell ferroptosis in SLE patients and SLE mouse models, suggesting that ferroptosis may regulate B cell differentiation and plasma cell formation, thereby implicating this process in SLE pathogenesis [102]
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This neurological involvement occurs partly through the methylmalonyl-CoA mutase pathway, where B12 deficiency leads to accumulation of methylmalonic acid that can damage nerve cells
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