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Shows that lncRNA Tug1 knockdown increases mitochondrial calcium uniporter expression via CaMKII in cardiomyocytes, suggesting a potential therapeutic target for cardiovascular disease.
Calcium is essential for signaling, excitation contraction, and energy homeostasis in the heart. Despite this, molecular regulators of these processes are not completely understood. We report that knockdown of lncRNA Tug1 alters the calcium handling transcriptome and increases mitochondrial calcium uniporter expression via a mechanism involving CaMKII. As overexpression of MCU is known to be protective against pathological cardiac remodeling, targeting Tug1 may be a potential strategy for treating cardiovascular disease.
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Trewin et al. (2023) studied this question.
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