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. Author manuscript; available in PMC: 2020 Jul 1.
Published in final edited form as: J Mol Cell Cardiol. 2019 Apr 28;132:1–12. doi: 10.1016/j.yjmcc.2019.04.023

Figure 1.

Figure 1

Signaling pathways that modulate cardioprotection in CMs. Mechanical and oxidative stress produced in disease or exercise can induce a complex anti-apoptotic and hypertrophic response in CMs that converges on the RhoA and PI3K/Akt signaling pathways. Stimulation of GPCRs through ligands triggers RhoA-dependent actin polymerization and nuclear localization of MRTFs to activate transcription of MRTF/SRF target genes. Expression of targets such as miR-486 and CCNs, as well as exercise-induced mechanical tension can activate the Akt response to contribute to cardioprotection. RhoA can also modulate the Hippo/YAP signaling pathway to regulate proliferation and stress responsive genes during both development and disease.