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The function of autophagy as a fundamental process of preserving cell homeostasis

By
Nikolina Elez-Burnjaković ,
Nikolina Elez-Burnjaković

Faculty of Medicine, Foca, University of East Sarajevo , Lukavica , Bosnia and Herzegovina

Lejla Pojskić ,
Lejla Pojskić

Institute for Genetic Engineering and Biotechnology, University of Sarajevo , Sarajevo , Bosnia and Herzegovina

Sanin Haverić ,
Sanin Haverić

Institute for Genetic Engineering and Biotechnology, University of Sarajevo , Sarajevo , Bosnia and Herzegovina

Ajla Smajlović
Ajla Smajlović

Institute for Genetic Engineering and Biotechnology, University of Sarajevo , Sarajevo , Bosnia and Herzegovina

Abstract

Autophagy is a dynamic process, conserved in all eukaryotes. It is responsible for the degradation of cytoplasmic content. Autophagy is crucial in cell survival and cell death. It plays a significant role in the cell response to stress, nutrient deficiencies, embryonic development, tumor suppression, response to pathogens and aging. The process of autophagy is also involved in the pathology of human diseases, such as cancer, diabetes, cardiomyopathy, and neurodegenerative diseases such as Alzheimer's and Parkinson's disease. Autophagy is a mechanism that involves degradation of cells, proteins, damaged organelles and pathogens through the lysosomal mechanisms, thus autophagy supports cell survival during starvation, hypoxia and metabolic stress. However, if extensive and/or excessive, autophagy can promote apoptosis (type I) or function as an alternative cell-death pathway, called autophagic cell death (type II). Autophagy can either promote cancer cell death, or serve as a survival mechanism against apoptosis or necrosis induced by various anticancer treatments. Given the contradictory role of autophagy during tumor initiation and progression, the use of autophagy in therapy depends on the context and must be approached individually

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Authors retain copyright. This work is licensed under a Creative Commons Attribution 4.0 International License. Creative Commons License

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