Affiliation:
1. Federal Research Center for Fundamental and Translational Medicine
2. Belarusian State University (BSU)
3. Novosibirsk State Pedagogical University
Abstract
Autophagy is the main catabolic process required for the removal of damaged organelles, aggregated proteins and intracellular pathogens from cells. Oxidative stress is accompanied by an increase in autophagy, which has a protective effect by maintaining the qualitative composition of mitochondria (mitophagy) and peroxisomes (pexophagy) followed by lysosomal degradation of organelles with high production of reactive oxygen species. Aggrephagy also removes toxic products formed during oxidative and carbonyl stress. Furthermore, autophagy can activate the antioxidant response element system and increase the expression of antioxidant enzyme genes. The protective role of autophagy can be useful in many pathological processes accompanied by the development of oxidative stress while at the same time it may cause chemoresistance, reducing the effectiveness of anti-tumor therapy.
Publisher
Siberian State Medical University
Reference139 articles.
1. Menshchikova E.B., Zenkov N.K., Lankin V.Z., Bondar’ I.A., Trufakin V.A. Oxidative stress. Pathological conditions and diseases. Novosibirsk: ARTA Publ., 2008: 284 (in Russ.)].
2. Lionaki E., Markaki M., Palikaras K., Tavernarakis N. Mitochondria, autophagy and age-associated neurodegenerative diseases: New insights into a complex interplay. Biochim. Biophys. Acta. 2015; 1847 (11): 1412–1423. DOI: 10.1016/j.bbabio.2015.04.010.
3. Men’shchikova Ye.B., Lankin V.Z., Kandalintseva N.V. Phenolic antioxidants in biology and medicine]. Saarbrücken: LAP LAMBERT Acad. Publishing Publ., 2012: 496 (in Russ.)].
4. Filomeni G., De Zio D., Cecconi F. Oxidative stress and autophagy: the clash between damage and metabolic needs. Cell Death Differ. 2015; 22 (3): 377–388. DOI: 10.1038/cdd.2014.150.
5. Galadari S., Rahman A., Pallichankandy S., Thayyullathil F. Reactive oxygen species and cancer paradox: To promote or to suppress? Free Radic. Biol. Med. 2017; 104: 144–164. DOI: 10.1016/j.freeradbiomed.2017.01.004.
Cited by
4 articles.
订阅此论文施引文献
订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献