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Further biochemical studies have shown increased levels of neuroketals in the SNc in post mortem tissue from Braak stages 1 and 2, supporting the notion that oxidative damage to specific lipids in the SNc occurs at very early stages of PD and prior to the appearance of LBP [83, 84]

log 2 FC = 20.46), a Ca 2+ regulator affecting acute kidney injury [39, 40], ERLINs, which regulate IP 3 receptors, DNAJs regulating degradation, and ARFs controlling G-protein coupled receptors (GPCRs)

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Consequently, designing therapies that promote the transformation of CAF subtypes from tumor-promoting to tumor-suppressive phenotypes has become an important direction for future research