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. 2020 Apr 8;11:267. doi: 10.3389/fphys.2020.00267

FIGURE 4.

FIGURE 4

(A) In the heart, ischemia/reperfusion activates ATF6, which (B) induces canonical ER stress-response genes, as well as non-canonical genes, such as the peroxisomal antioxidant, catalase, which resides in peroxisomes and protects from the ROS that are generated during I/R. (C) In the heart, growth stimuli activate ATF6, which (D) induces canonical ER stress-response genes, as well as non-canonical genes, such as the small GTP-binding protein, Rheb, which is an activator of the growth-promoting kinase complex, mTORC1. (E,F) In the heart, different stimuli induce different ATF6-dependent genes. For example, (E) oxidative stress induces catalase but not rheb, and catalase protects the heart from damage, while (F) growth stimuli induce rheb but not catalase, which is required for physiological and pathological hypertrophic growth of the heart. (G,H) The absence of induction of any of these genes when ATF6 is deleted from cardiac myocytes supports the view that gene induction by both oxidative stress and growth stimuli is dependent upon ATF6.