@Article{biocell.2026.082978,
AUTHOR = {Yi Lu, Lixiang Wang, Jiaheng Xu, Heru Wang, Jiayu Li, Wanshun Li, Xinyi Su, Hongyu Li, Deyu Zhang, Zhendong Jin, Haojie Huang},
TITLE = {The Autophagy-Oxidative Stress Circuit: A Conductor of Cell Fate},
JOURNAL = {BIOCELL},
VOLUME = {},
YEAR = {},
NUMBER = {},
PAGES = {{pages}},
URL = {http://www.techscience.com/biocell/online/detail/27173},
ISSN = {1667-5746},
ABSTRACT = {Autophagy and oxidative stress form a bidirectional and dynamic regulatory network governing cell fate. Dysregulation of this crosstalk contributes to the pathogenesis of various diseases, including cancer, neurodegeneration, inflammation, metabolic disorders, and aging. Therefore, a deep understanding of the molecular mechanisms underlying the interplay between autophagy and oxidative stress provides a theoretical foundation for developing therapeutic strategies targeting this axis. This review synthesizes recent literature on the underlying molecular mechanisms. Oxidative stress drives autophagic initiation through multiple interconnected pathways, including direct oxidative modification of core autophagy-related proteins, modulation of canonical signaling cascades, activation of nuclear transcription factors, and induction of selective autophagy. In turn, autophagy acts as a pivotal cytoprotective mechanism by eliminating reactive oxygen species (ROS) generated by damaged organelles, sustaining metabolic homeostasis, and reinforcing antioxidant signaling, thereby counteracting oxidative damage. The balance between these two processes determines whether cells adapt and survive, undergo programmed cell death, or enter senescence.},
DOI = {10.32604/biocell.2026.082978}
}