About the book
In eukaryotic cells, the endoplasmic reticulum is an organelle adjacent to the nuclear membrane. This organelle is essential for calcium homeostasis and lipid biosynthesis and protein assembly, folding, and post-translational modification. The interplay between the endoplasmic reticulum membrane and the outer mitochondrial membrane, called mitochondria-associated endoplasmic reticulum membranes (MAMs), permits a wide range of cellular activity, including the division and fusion of mitochondria and the dynamic passage of lipids, glycogen, and calcium ions.
It has been established that energy/nutrient depletion, calcium flux injury, or oxidative stress disrupt endoplasmic reticulum homeostasis and even induce accumulation of misfolded/unfolded proteins leading to endoplasmic reticulum stress. Under endoplasmic reticulum stress conditions, an adaptive mechanism of coordinated signaling pathways, defined unfolded protein response (UPR), is activated to return the endoplasmic reticulum to its healthy functioning state. The aging causes a decrease of the protective adaptive response of the UPR and an increase of the pro-apoptotic pathway together with endoplasmic reticulum ultrastructural injury. Controlling endoplasmic reticulum stress response, maintaining the appropriate endoplasmic reticulum ultrastructure and homeostasis, and retaining mitochondria interplay are crucial aspects for cellular health.
This book presents a comprehensive overview of endoplasmic reticulum, including, but not limited to, endoplasmic reticulum ultrastructural anatomy, MAMs, endoplasmic reticulum stress, and their implication in health and diseases. Additionally, identifying perturbations in the endoplasmic reticulum stress response could lead to early detection of age-related disease and may help develop therapeutic approaches.
