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developed a biomimetic nanomodulator targeting sepsis-associated encephalopathy, which crossed the blood-brain barrier, alleviated oxidative stress, polarized macrophages toward anti-inflammatory phenotypes, and improved cognition and survival (Qu et al., 2024)
Notably, overexpression of ubiquitin-specific protease 48 (USP48) can inhibit the above pathological processes by deubiquitinating SLC1A5, suggesting that targeting the ferroptosis-inflammation axis represents a promising potential strategy for DR treatment (168)
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