| Chaudhari, N., Talwar, P., Parimisetty, A., & others. (2014). A Molecular Web: Endoplasmic Reticulum Stress, Inflammation, and Oxidative Stress. Front. Cell. Neurosci. 8. |
 
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| Last edited by: Dr. Enrique Feoli 2021-02-27 18:26:14 |
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 A loop of oxidative stress, ER stress leading to inflammation. During protein overload, ROS are generated in the ER as a part of an oxidative folding process during electron transfer between protein disulfide isomerase (PDI) and endoplasmic reticulum oxidoreductin-1 (ERO-1). ROS can target ER resident proteins, enzymes, and chaperones (not shown) and ER based calcium (Ca2+) channels, leading to the release of calcium from the ER into the cytosol and ER-stress signaling. Increased cytosolic calcium and calcium entry in mitochondria from ER via MAM-associated channels can stimulate mitochondria metabolism to produce more ROS. Increased mitochondrial calcium concentration causes cytochrome c release, altered membrane potential that eventually triggers cellular death programs. The increased protein folding demand, calcium and ROS signaling integrates with UPR pathways and can potentially lead to inflammatory responses. |
