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Firstly, the majority of existing studies are based on animal models or in vitro experiments, which may not fully translate to the human disease context in terms of the significance and regulatory mechanisms of ferroptosis
(2007) have pointed out that the pathophysiology of DCVC-induced acute tubular necrosis followed by acute renal failure in mice and clinical acute renal failure in patients is similar
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The B cells then start producing antibodies against gliadin, the bodys own tissue transglutaminase (anti-TG2-Ab), and endomysium (anti-EMA) [28]
