Oxidative stress and mitochondrial dysfunction play critical roles in ischemia/reperfusion (I/R) injury. DJ-1 is an endogenous antioxidant that attenuates oxidative stress and maintains mitochondrial function, likely acting as a protector of I/R injury. In the present study, we explored the protective effect of a possible DJ-1 agonist, sodium phenylbutyrate (SPB), against I/R injury by protecting mitochondrial dysfunction the upregulation of DJ-1 protein.
View Article and Find Full Text PDFCalcium (Ca) dyshomeostasis induced by endoplasmic reticulum (ER) stress is an important molecular mechanism of selective dopaminergic (DA) neuron loss in Parkinson's disease (PD). Inositol 1,4,5-triphosphate receptors (IPRs) and ryanodine receptors (RyRs), which are located on the ER surface, are the main endogenous Ca release channels and play crucial roles in regulating Ca homeostasis. However, the roles of these endogenous Ca release channels in PD and their effects on the function and survival of DA neurons remain unknown.
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