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. 2020 Dec 23;8(6):891–906. doi: 10.1016/j.gendis.2020.12.006

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© 2020 Chongqing Medical University. Production and hosting by Elsevier B.V.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 8 — Schematic representation of PGC-1α regulates mitochondrial metabolism and molecular mechanism during cardiac differentiation and maturation. After hiPSCs differentiated into hiPSC-CMs, mitochondrial biogenesis and metabolism is improved, concomitantly with the increase of PGC-1α expression. Upregulating PGC-1α by ZLN005 further promote mitochondrial oxidation function though regulating its downstream proteins, particularly ERRα. Besides regulated by PGC-1α, ERRα interacts with it and is required in the PGC-1α-introduced mitochondrial biogenesis and metabolism in hiPSC-CMs.