Reactive oxygen species–autophagy axis (ROS–autophagy axis)

The Reactive oxygen species (ROS)–autophagy axis represents a complex regulatory feedback loop where ROS serve as key signaling molecules to initiate or modulate autophagic activity. Under conditions of oxidative stress, ROS can activate autophagy through various mechanisms, including the regulation of Atg proteins, the inhibition of the mTOR pathway, or the activation of the AMPK pathway (Filomeni et al., 2015, Trends in Molecular Medicine). This axis is fundamental for maintaining cellular quality control by facilitating the degradation of damaged mitochondria (mitophagy) and oxidized proteins, thereby preventing further ROS accumulation. In the context of disease, the ROS–autophagy axis is often dysregulated; in cancer, it can act as a double-edged sword, either promoting tumor cell survival under metabolic stress or inducing autophagic cell death (Scherz-Shouval & Elazar, 2011, Antioxidants & Redox Signaling). Pharmacological intervention targeting this axis includes the use of antioxidants like N-acetylcysteine to reduce ROS-driven autophagy or autophagy modulators like Rapamycin and Chloroquine to alter the downstream response (Li et al., 2012, Autophagy).

Other names

ROS-induced autophagyOxidative stress-autophagy pathwayRedox-autophagy signaling

Modulation of intracellular redox state and autophagic flux to restore cellular homeostasis or induce programmed cell death.