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756 Overexpression of ACSL4 exacerbates cerebral I/R injury in rodents, while genetic or pharmacological reduction of ACSL4 effectively prevents cerebral I/R injury
Revealing this mechanism reveals new mechanisms of gut-joint crosstalk of OA and offers a groundbreaking theoretical base for prevention and treatment of OA through bowel-inducing the behavioral change for OA by intervening BAMs signaling or ferroptosis inhibition
5.1.3.3 Traumatic brain injury TBI is characterized by structural or functional brain damage caused by external forces, and ferroptosis, a form of programmed cell death, is closely associated with TBI
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