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Rodents overexpressing USP22 or lncRNA PART1 were well resistant to I/R-induced oxidative stress and cardiac injury, which may be partly attributed to the elevated GSH content in the myocardium [251, 252]

These findings suggest that after the loss of dopaminergic neurons, a vicious cycle of decreased dopamine releaseDRD2 signaling deficiencydecreased GSH synthesisoxidative stressdopaminergic neuron death will occur, leading to GSH deficiency and the progression of PD

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Calreticulin Induced Endothelial ICAM-1 Up-Regulation Associated With Tristetraprolin Expression Alteration Through PI3K/Akt/eNOS/p38 MAPK Signaling Pathway in Rheumatoid Arthritis