Endoplasmic Reticulum Stress and Parkinson’s Disease: The Role of HRD1 in Averting Apoptosis in Neurodegenerative Disease

Figure 4

Therapeutic strategies for PD involving ER stress. (i) Addition of chemical chaperones (e.g., 4-PBA and tauroursodeoxycholic acid) or molecular inducers of ER chaperones (e.g., BIX); these molecules promote the appropriate folding of proteins and suppress the accumulation of unfolded proteins and ER stress-induced cell death, resulting in the prevention of neurodegeneration in PD, and (ii) the upregulation of ubiquitin ligase HRD1, its stabilizer SEL1L, or other ERAD components; HRD1 and its components promote the degradation of unfolded proteins and suppress ER stress-induced cell death, resulting in the prevention of neurodegeneration in PD.