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. 2022 Jan 13;9(2):998–1007. doi: 10.1002/ehf2.13725

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© 2021 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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CRKL plays a protective role in H/R‐induced cardiomyocyte injury. (A,B) Subcellular fractionation and FISH assays were conducted to identify the cellular location of circ_0001206. (C) CRKL expression was detected in H/R‐induced H9C2 cells upon circ_0001206 overexpression using quantitative real‐time polymerase chain reaction (RT‐qPCR) and western blot. (D) The efficacy of pcDNA3.1‐CRKL was tested by RT‐qPCR in hypoxia/reoxygenation (H/R)‐treated H9C2 cells. (E) Cell viability was tested in H/R‐induced H9C2 cells upon CRKL overexpression. (F) Western blot detected the protein levels of Bax, Bcl‐3, cleaved caspase‐3, and cleaved caspase‐9 in H/R‐induced H9C2 cells transfected with pcDNA3.1‐CRKL (n = 3). **P < 0.01.