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[178] established inducible cardiomyocyte‐specific deletion of Bmal1 in mice and reported that the loss of Bmal1 in cardiomyocytes resulted in a disrupted circadian pattern of the expression of Kcnh2, a K(+) channel gene, leading to prolonged ventricular repolarization
excludeInt
Variation:2 Gallon Cans
This framing complements broader or single-disease reviews (e.g., Wendorff-Tobolla et al., 2023b
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