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Mackenzie B, Erickson JD
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RIP1/RIP3-regulated necroptosis as a target for multifaceted disease therapy (Review)
This platform not only inhibits p38 MAPK phosphorylation to suppress inflammatory signaling but also scavenges hydroxyl radical (OH) and superoxide anion radical (O 2 ) via a tyrosinase-mimetic catalytic domain, while activating the SLC7A11/GPX4 axis to effectively attenuate ferroptosis [12]
Modification changes in the tumor cells themselves and changes in the immune microenvironment lead to complexity of the immune escape process
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