therapeutic interventions for endoplasmic reticulum stress
The endoplasmic reticulum (ER) is a subcellular organelle that is responsible for numerous functions including calcium homeostasis, protein secretion and lipid biosynthesis. However, cell death signaling pathways can be activated by prolonged stress to the ER originating from sources ranging from hypoxia, oxidative injury, high-fat diet, hypoglycaemia, protein inclusion bodies and viral infection. In fact, a number of disease processes are mediated and propagated through ER stress that lead to initiation of apoptosis. As increasing insight has been gained into the molecular mechanisms regulating ER stress and subsequent cell death, the potential for therapeutic benefit has been realized.
Why is this cool? ER-specific processes have been found to contribute or cause many diseases including Alzheimers, prion disease, Parkinson’s, heart disease, diabetes, cancer and autoimmune diseases. The ER is currently a novel therapeutic target and represents an avenue for considerable future impact. And as drugs are now being developed to target ER stress, we will see a lot of diseases being treated much more effectively than now. For more information, here is a review of molecular mechanisms for handling ER stress and subsequent activation of apoptosis as well as the clinical implications of this information.
