New insights into the interplay between autophagy and oxidative and endoplasmic reticulum stress in neuronal cell death and survival

Abstract

Autophagy is a dynamic process that maintains the normal homeostasis of cells by digesting and degrading aging proteins and damaged organelles. The effect of autophagy on neural tissue is still a matter of debate. Some authors suggest that autophagy has a protective effect on nerve cells, whereas others suggest that autophagy also induces the death of nerve cells and aggravates nerve injury. In mammals, oxidative stress, autophagy and endoplasmic reticulum stress (ERS) constitute important defense mechanisms to help cells adapt to and survive the stress conditions caused by physiological and pathological stimuli. Under many pathophysiological conditions, oxidative stress, autophagy and ERS are integrated and amplified in cells to promote the progress of diseases. Over the past few decades, oxidative stress, autophagy and ERS and their interactions have been a hot topic in biomedical research. In this review, we summarize recent advances in understanding the interactions between oxidative stress, autophagy and ERS in neuronal cell death and survival.

Discovery of Novel Isoquinoline Analogues as Dual Tubulin Polymerization/V-ATPase Inhibitors with Immunogenic Cell Death Induction

“…A great number of studies suggested that overproduction of ROS was also closely associated with ERS . In addition, there was extensive cross-talk between autophagy and ERS and the deficiency of autophagy flux could stimulate ERS activation and augment ERS-induced cell injury. , Therefore, the effect of F10 on ER deserves further analysis. The phosphorylation of eIF2α at Ser10 is essential for the ERS response; in addition, studies strongly support the view that phosphorylation of eIF2α is a specific marker of ICD .…”

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“…During the process of lysosome-dependent autophagy, damaged organelles, aggregated proteins, and degraded cytoplasmic debris accumulate within autophagic vacuoles ( Gao et al ., 2022 ; Zhang et al ., 2022 ). Autophagy has been recognized to play roles in the regulatory and developmental phases of lung damage.…”

“…PM obstructs the mammalian target of rapamycin (mTOR), a cellular nutritional status sensor, and intensifies cellular oxidative stress, culminating in cellular apoptosis and autophagy, causing the breakdown of cellular components ( Yan et al ., 2021 ). Autophagy, a crucial lysosome-dependent mechanism that contributes to cellular homeostasis, has been connected to protein aggregation, organelle impairment, and the clearance of intracellular pathogens ( Gao et al ., 2022 ). Furthermore, autophagy’s implications in lung-related conditions underscore its significance in managing pulmonary disorders ( Zhang et al ., 2022 ).…”

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