Oxidative stress and autophagy: the clash between damage and metabolic needs
By G. Filomeni, D. Zio, F. Cecconi. Cell Death and Differentiation, 2014
2,029 citations recorded by the source corpus.
Autophagy is a catabolic process aimed at recycling cellular components and damaged organelles in response to diverse conditions of stress, such as nutrient deprivation, viral infection and genotoxic stress. A growing amount of evidence in recent years argues for oxidative stress acting as the converging point of these stimuli, with reactive oxygen species (ROS) and reactive nitrogen species (RNS) being among the main intracellular signal transducers sustaining autophagy. This review aims at providing novel insight into the regulatory pathways of autophagy in response to glucose and amino acid deprivation, as well as their tight interconnection with metabolic networks and redox homeostasis. The role of oxidative and nitrosative stress in autophagy is also discussed in the light of its being harmful for both cellular biomolecules and signal mediator through reversible posttranslational modifications of thiol-containing proteins. The redox-independent relationship between autophagy and antioxidant response, occurring through the p62/Keap1/Nrf2 pathway, is also addressed in order to provide a wide perspective upon the interconnection between autophagy and oxidative stress. Herein, we also attempt to afford an overview of the complex crosstalk between autophagy and DNA damage response (DDR), focusing on the main pathways activated upon ROS and RNS overproduction. Along these lines, the direct and indirect role of autophagy in DDR is dissected in depth.
Subfields: Epidemiology, Geriatrics and Gerontology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/9c073d5a36cc35bf3874d5a9489a6cb43064c19e
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Citations in the corpus
- Reactive oxygen species and mitochondria: A nexus of cellular homeostasis (2015, background): “However, it is commonly accepted that the principal sources of ROS in the cell during infection are NOX2 and the ETC of mitochondria [61].”
- NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential (2020, background): “94,134 Therefore, through supplying electrons for bioreductive synthesis and the regeneration of GSH and reduced thioredoxin, NADPH plays critical roles in the maintenance of redox homeostasis and modulating redox signaling.(133)”
- ROS, Cell Senescence, and Novel Molecular Mechanisms in Aging and Age-Related Diseases (2016, background): “ROS is integral in the development of physiopathologic events like mitochondrial death signaling [86] and autophagy [87], besides inflammation and infection [55, 88], in which they impart immunological changes.”
- The Roles of Autophagy in Cancer (2018, background): “mitochondria induces excessive ROS production, resulting in promotion of carcinogenesis [68,69,70].”