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We thank Ilona Ungi and Judit Pipis for the excellent technical support during the operations. The work and publication were supported by the projects GINOP-2.3.2-15-2016-00006, NKFIH K115990, and the Ministry of Human Capacities, Hungary (20391-3/2018/FEKUSTRAT. M. Sarkozy was supported by the Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences. M. Sarkozy and M.G. Kovacs were supported by the New National Excellence Program of the Ministry of Human Capacities (UNKP-17-4-I-SZTE-43, UNKP-17-2-I-SZTE-30, UNKP-18-4-SZTE-63, UNKP-18-3-II-SZTE-15). F. Marvanykovi was supported by the Szeged Scientists Academy Program. 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"firstPageOrInternalIdForSort" : "1302", "pageLength" : 16, "publishedYear" : 2019, "abstractText" : "Chronic kidney disease (CKD) is a public health problem that increases the risk of cardiovascular morbidity and mortality. Heart failure with preserved ejection fraction (HFpEF) characterized by left ventricular hypertrophy (LVH) and diastolic dysfunction is a common cardiovascular complication of CKD. MicroRNA-212 (miR-212) has been demonstrated previously to be a crucial regulator of pathologic LVH in pressure-overload-induced heart failure via regulating the forkhead box O3 (FOXO3)/calcineurin/nuclear factor of activated T-cells (NFAT) pathway. Here we aimed to investigate whether miR-212 and its hypertrophy-associated targets including FOXO3, extracellular signal-regulated kinase 2 (ERK2), and AMP-activated protein kinase (AMPK) play a role in the development of HFpEF in CKD. CKD was induced by 5/6 nephrectomy in male Wistar rats. Echocardiography and histology revealed LVH, fibrosis, preserved systolic function, and diastolic dysfunction in the CKD group as compared to sham-operated animals eight and/or nine weeks later. Left ventricular miR-212 was significantly overexpressed in CKD. However, expressions of FOXO3, AMPK, and ERK2 failed to change significantly at the mRNA or protein level. The protein kinase B (AKT)/FOXO3 and AKT/mammalian target of rapamycin (mTOR) pathways are also proposed regulators of LVH induced by pressure-overload. Interestingly, phospho-AKT/total-AKT ratio was increased in CKD without significantly affecting phosphorylation of FOXO3 or mTOR. In summary, cardiac overexpression of miR-212 in CKD failed to affect its previously implicated hypertrophy-associated downstream targets. 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