Abstract

Autophagy and DNA repair are two essential biological mechanisms that maintain cellular homeostasis. Impairment of these mechanisms was associated with several pathologies such as premature aging, neurodegenerative diseases, and cancer. Intrinsic or extrinsic stress stimuli (e.g., reactive oxygen species or ionizing radiation) cause DNA damage. As a biological stress response, autophagy is activated following insults that threaten DNA integrity. Hence, in collaboration with DNA damage repair and response mechanisms, autophagy contributes to the maintenance of genomic stability and integrity. Yet, connections and interactions between these two systems are not fully understood. In this review article, current status of the associations and crosstalk between autophagy and DNA repair systems is documented and discussed.

Highlights

  • Maintenance of cellular homeostasis in living organisms requires a balance between anabolic and catabolic reactions

  • We briefly describe autophagy and DNA repair pathways and dissect molecular and cellular outcomes of interactions and crosstalk between these pathways

  • Cdmediated DNA damage-induced autophagy through the inhibition of mTOR by AMPK which activated upon the increased level of Ataxia-telangiectasia mutated (ATM) (Li et al, 2017)

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Summary

Introduction

Maintenance of cellular homeostasis in living organisms requires a balance between anabolic and catabolic reactions. Autophosphorylation of ULK1 further promotes its activity and induces phosphorylation of several autophagy proteins, including ATG13 and FIP200 (Hosokawa et al, 2009); mTOR complexes are found to be associated with lysosomes where autophagic cargos are degraded. DDR is a complex cellular mechanism which involves the activation of several molecules that are stimulated in response to DNA damages (Matt and Hofmann, 2016).

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