z-logo
Premium
Crosstalk of autophagy and apoptosis: Involvement of the dual role of autophagy under ER stress
Author(s) -
Song Shuling,
Tan Jin,
Miao Yuyang,
Li Mengmeng,
Zhang Qiang
Publication year - 2017
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.25785
Subject(s) - autophagy , microbiology and biotechnology , unfolded protein response , atf6 , atg5 , endoplasmic reticulum , apoptosis , crosstalk , biology , programmed cell death , signal transduction , homeostasis , dual role , cellular stress response , chemistry , biochemistry , fight or flight response , physics , gene , optics , combinatorial chemistry
Endoplasmic reticulum (ER) stress is a common cellular stress response that is triggered by a variety of conditions that disturb cellular homeostasis, and induces cell apoptosis. Autophagy, an important and evolutionarily conserved mechanism for maintaining cellular homeostasis, is closely related to the apoptosis induced by ER stress. There are common upstream signaling pathways between autophagy and apoptosis induced by ER stress, including PERK/ATF4, IRE1α, ATF6, and Ca 2+ . Autophagy can not only block the induction of apoptosis by inhibiting the activation of apoptosis‐associated caspase which could reduce cellular injury, but also help to induce apoptosis. In addition, the activation of apoptosis‐related proteins can also inhibit autophagy by degrading autophagy‐related proteins, such as Beclin‐1, Atg4D, Atg3, and Atg5. Although the interactions of different autophagy‐ and apoptosis‐related proteins, and also common upstream signaling pathways have been found, the potential regulatory mechanisms have not been clearly understood. In this review, we summarize the dual role of autophagy, and the interplay and potential regulatory mechanisms between autophagy and apoptosis under ER stress condition.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here