@article{10.1172/jci.insight.138027, author = {Jingfu Bao AND Yinghui Lu AND Qinying She AND Weijuan Dou AND Rong Tang AND Xiaodong Xu AND Mingchao Zhang AND Ling Zhu AND Qing Zhou AND Hui Li AND Guohua Zhou AND Zhongzhou Yang AND Shaolin Shi AND Zhihong Liu AND Chunxia Zheng}, journal = {JCI Insight}, publisher = {The American Society for Clinical Investigation}, title = {MicroRNA-30 regulates left ventricular hypertrophy in chronic kidney disease}, year = {2021}, month = {5}, volume = {6}, url = {https://insight.jci.org/articles/view/138027}, abstract = {Left ventricular hypertrophy (LVH) is a primary feature of cardiovascular complications in patients with chronic kidney disease (CKD). miRNA-30 is an important posttranscriptional regulator of LVH, but it is unknown whether miRNA-30 participates in the process of CKD-induced LVH. In the present study, we found that CKD not only resulted in LVH but also suppressed miRNA-30 expression in the myocardium. Rescue of cardiomyocyte-specific miRNA-30 attenuated LVH in CKD rats without altering CKD progression. Importantly, in vivo and in vitro knockdown of miRNA-30 in cardiomyocytes led to cardiomyocyte hypertrophy by upregulating the calcineurin signaling directly. Furthermore, CKD-related detrimental factors, such as fibroblast growth factor-23, uremic toxin, angiotensin II, and transforming growth factor–β, suppressed cardiac miRNA-30 expression, while miRNA-30 supplementation blunted cardiomyocyte hypertrophy induced by such factors. These results uncover a potentially novel mechanism of CKD-induced LVH and provide a potential therapeutic target for CKD patients with LVH.}, number = {10}, doi = {10.1172/jci.insight.138027}, url = {https://doi.org/10.1172/jci.insight.138027}, }