The Dual Role of Oxidative-Stress-Induced Autophagy in Cellular Senescence: Comprehension and Therapeutic Approaches
Pavlos Pantelis,
George Theocharous,
Nefeli Lagopati,
Dimitris Veroutis,
Dimitris-Foivos Thanos,
Giasemi-Panagiota Lampoglou,
Natassa Pippa,
Maria-Anna Gatou,
Ioanna Tremi,
Angelos Papaspyropoulos,
Efthymios Kyrodimos,
Evangelia A. Pavlatou,
Maria Gazouli,
Konstantinos Evangelou,
Vassilis G. Gorgoulis
Affiliations
Pavlos Pantelis
Molecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece
George Theocharous
Molecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece
Nefeli Lagopati
Molecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece
Dimitris Veroutis
Molecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece
Dimitris-Foivos Thanos
Molecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece
Giasemi-Panagiota Lampoglou
Molecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece
Natassa Pippa
Section of Pharmaceutical Technology, Department of Pharmacy, School of Health Sciences, National and Kapodistrian University of Athens, 15771 Athens, Greece
Maria-Anna Gatou
Laboratory of General Chemistry, School of Chemical Engineering, National Technical University of Athens, 6 Zografou Campus, 15789 Zografou, Greece
Ioanna Tremi
Molecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece
Angelos Papaspyropoulos
Molecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece
Efthymios Kyrodimos
First ENT Department, Hippocration Hospital, University of Athens, 11527 Athens, Greece
Evangelia A. Pavlatou
Laboratory of General Chemistry, School of Chemical Engineering, National Technical University of Athens, 6 Zografou Campus, 15789 Zografou, Greece
Maria Gazouli
Laboratory of Biology, Department of Basic Medical Sciences, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece
Konstantinos Evangelou
Molecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece
Vassilis G. Gorgoulis
Molecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece
The contemporary lifestyle of the last decade has undeniably caused a tremendous increase in oxidative-stress-inducing environmental sources. This phenomenon is not only connected with the rise of ROS levels in multiple tissues but is also associated with the induction of senescence in different cell types. Several signaling pathways that are associated with the reduction in ROS levels and the regulation of the cell cycle are being activated, so that the organism can battle deleterious effects. Within this context, autophagy plays a significant role. Through autophagy, cells can maintain their homeostasis, as if it were a self-degradation process, which removes the “wounded” molecules from the cells and uses their materials as a substrate for the creation of new useful cell particles. However, the role of autophagy in senescence has both a “dark” and a “bright” side. This review is an attempt to reveal the mechanistic aspects of this dual role. Nanomedicine can play a significant role, providing materials that are able to act by either preventing ROS generation or controllably inducing it, thus functioning as potential therapeutic agents regulating the activation or inhibition of autophagy.
