Knockdown of HMGB1 suppressed high glucose-induced activation of TLR4/NF-κB axis and promoted Nrf2 expression as well as its downstream targets, including HO−1, NAD(P)H dehydrogenase (quinone 1) (NQO-1), glutamate–cysteine ligase catalytic subunit (GCLC), and glutamate–cysteine ligase modifier subunit (GCLM) in mesangial cells in vitro [81], which suggested that targeting HMGB1 for ferroptosis might be a novel therapeutic strategy in diabetic kidney disease. Here, HMGB1 is linked to diabetic kidney disease.