Autophagy is an evolutionarily conserved catabolic process that is induced in response to various stress factors in order to protect cells and maintain cellular homeostasis by degrading redundant components and dysfunctional organelles. Dysregulation of autophagy has been implicated in several conditions such as cancer, neurodegenerative diseases, and metabolic disorders. Although autophagy has been commonly considered as a cytoplasmic process, accumulating evidence has revealed that epigenetic regulation within the nucleus is also important for regulation of autophagy. In particular, when energy homeostasis is disrupted, for instance due to nutrient deprivation, cells increase autophagic activity at the transcriptional level, thereby also increasing the extent of overall autophagic flux. The transcription of genes associated with autophagy is strictly regulated by epigenetic factors through a network of histone-modifying enzymes along with histone modifications. A better understanding of the complex regulatory mechanisms of autophagy could reveal potential new therapeutic targets for autophagy-related diseases. In this review, we discuss the epigenetic regulation of autophagy in response to nutrient stress, focusing on histone-modifying enzymes and histone modifications.
Bibliographical noteFunding Information:
Figures in this review were created using BioRender.com. Creative Research Initiatives Program (Research Center for Epigenetic Code and Diseases) [2017R1A3B1023387 to SHB]; Science Research Center Program (Cellular Heterogeneity Research Center) [NRF-RS-2023-00207857 to KIK]; Basic Science Research Program [NRF-2021R1A2C1006680 to KIK]; Basic Science Research Program [NRF-2022R1A2C2010940 to HK]; Sejong Science Fellowship Program [NRF-2021R1C1C2010332 to YSY] from the National Research Foundation (NRF) grant funded by the Korea government.
© 2023, The Author(s), under exclusive licence to ADMC Associazione Differenziamento e Morte Cellulare.
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology