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Review

The role of the unfolded protein response in arrhythmias

& ORCID Icon
Pages 335-345 | Received 10 Aug 2018, Accepted 22 Aug 2018, Published online: 29 Sep 2018

Figures & data

Figure 1. The scheme of the unfolded protein response (UPR) signaling cascades and functions.

Figure 1. The scheme of the unfolded protein response (UPR) signaling cascades and functions.

Figure 2. Tunicamycin-induced UPR activation alters the morphology of the action potential with prolonged action potential duration and decreased dV/dtmax of hiPSC-CMs, by decreasing all major cardiac ion channel currents.

Figure 2. Tunicamycin-induced UPR activation alters the morphology of the action potential with prolonged action potential duration and decreased dV/dtmax of hiPSC-CMs, by decreasing all major cardiac ion channel currents.

Figure 3. A summarized scheme of the UPR regulation on human cardiac ion channels. Activated UPR downregulates selective ion channels, leads to prolonged APD and reduced dV/dtmax, which can contribute to electrical remodeling and arrhythmias. The PERK branch downregulates Nav1.5, Kv4.3, hERG, and KvLQT1, while the IRE1 branch downregulates Nav1.5, Cav1.2, hERG, and KvLQT1.

Figure 3. A summarized scheme of the UPR regulation on human cardiac ion channels. Activated UPR downregulates selective ion channels, leads to prolonged APD and reduced dV/dtmax, which can contribute to electrical remodeling and arrhythmias. The PERK branch downregulates Nav1.5, Kv4.3, hERG, and KvLQT1, while the IRE1 branch downregulates Nav1.5, Cav1.2, hERG, and KvLQT1.

Figure 4. A summary of the UPR activation causing arrhythmias.

Figure 4. A summary of the UPR activation causing arrhythmias.