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The accumulation of misfolded protein in the endoplasmic reticulum (ER) leads to ER dysfunction, which is known as ER stress ( 12 regulated ER homeostasis ( 12 deficiency activated ER stress pathways by increasing the phosphorylation of PERK and IRE1 and the expression of ATF6 ( 12 could promote nerve regeneration after TBI by regulating ER stress

4 FSP1 protects against unrestrained lipid peroxidation in a COQ2-dependent manner

Chronic conditions that took years to develop will not resolve in days

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In addition to these sources, inflammatory processes in the body are significant contributors to free radical production [8]

As a result, red blood cells grow too big and dont work well