Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy

Abstract

Oxidative stress is an imbalance between free radicals and the antioxidant system causing overgeneration of free radicals (oxygen-containing molecules) ultimately leading to oxidative damage in terms of lipid peroxidation, protein denaturation, and DNA mutation. Oxidative stress can activate autophagy to alleviate oxidative damage and maintain normal physiological activities of cells by degrading damaged organelles or local cytoplasm. When oxidative stress is not eliminated by autophagy, it activates the apoptosis cascade. This review provides a brief summary of mitochondrial-endoplasmic reticulum communication-mediated oxidative stress and autophagy. Mitochondria and endoplasmic reticulum being important organelles in cells are directly or indirectly connected to each other through mitochondria-associated endoplasmic reticulum membranes and jointly regulate oxidative stress and autophagy. The reactive oxygen species (ROS) produced by the mitochondrial respiratory chain are the main inducers of oxidative stress. Damaged mitochondria can be effectively cleared by the process of mitophagy mediated by PINK1/parkin pathway, Nix/BNIP3 pathways, and FUNDC1 pathway, avoiding excessive ROS production. However, the mechanism of mitochondrial-endoplasmic reticulum communication in the regulation of oxidative stress and autophagy is rarely known. For this reason, this review explores the mutual connection of mitochondria and endoplasmic reticulum in mediating oxidative stress and autophagy through ROS and Ca 2+ and aims to provide part of the theoretical basis for alleviating oxidative stress through autophagy mediated by mitochondrial-endoplasmic reticulum communication.

Recent progress of oxidative stress associated biomarker detection

“…Oxidative stress, the imbalance between the production of reactive oxygen species (ROS) and antioxidant defenses in biological systems, plays an important role in the physiological and pathological processes of diseases. [1][2][3] ROS, as versatile signal molecules, are of vital significance in maintaining cell redox homeostasis and mediating intracellular signal pathways. 4,5 Under physiological conditions, the generation and elimination of ROS in organisms are always in a dynamic equilibrium state.…”

Neuroprotective effect of short‐chain fatty acids against oxidative stress‐induced SH‐SY5Y injury via GPR43‐dependent pathway

“…An increase in intracellular calcium from G q activation further prevents the increase in the ratio between pro‐apoptotic protein and antiapoptotic protein expression (Bcl‐2) from H 2 O 2 ‐induced neuronal injury. It is known that an increase in the level of intracellular reactive oxygen species can induce neuronal death by increasing the mitochondrial stress that triggers the apoptosis process (Forman & Zhang, 2021; Liu et al, 2022). As a result, one possible protective mechanism of SCFAs mixture via GPR43 activation is (1) a lower level of reactive oxygen species within the cell, (2) protection of mitochondria from oxidative stress, and (3) prevention of the downstream activation of the apoptosis signaling pathway.…”

Interplay of human gastrointestinal microbiota metabolites: Short-chain fatty acids and their correlation with Parkinson’s disease

“…This disrupts the redox balance within cells, leading to oxidative stress and irreversible cellular damage. [92,103,104] Given the heightened activity of neurons in the human body, mitochondrial dysfunction and oxidative stress emerge as pivotal contributing factors to PD. Commonly used induction mechanisms in PD animal models involve oxidative stress-induced damage to dopaminergic neurons in the substantia nigra.…”