ArticleScientific reports2019
Chronic kidney disease induces left ventricular overexpression of the pro-hypertrophic microRNA-212.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- Beyond Blood Pressure: Cardiac Structural and Functional Abnormalities in Hypertensive Postmenopausal Women with Mild-to-Moderate Chronic Kidney Disease.Journal of clinical medicine · 2026Article
- E/e' ratio combined with left ventricular mass index predicts HFpEF rehospitalization risk in stage 3-4 chronic kidney disease patients: a retrospective cohort study.Frontiers in cardiovascular medicine · 2026Article
- Beyond Traditional Silos: An Integrated Framework Leveraging Novel Pathways for Reducing Cardio-renal Risk in Type 2 Diabetes.Current diabetes reviews · 2026Review
- Roles of microRNAs in cardiorenal syndrome.Molecular and cellular biochemistry · 2025Review
- Differential Myocardial Responses in Male and Female Rats with Uremic Cardiomyopathy.International journal of molecular sciences · 2025Article
- Benefit of combination therapy with dapagliflozin and eplerenone on cardiac function and fibrosis in rats with non-diabetic chronic kidney disease.Scientific reports · 2024Article
- Nonsteroidal Mineralocorticoid Receptor Antagonist Finerenone Improves Diastolic Dysfunction in Preclinical Nondiabetic Chronic Kidney Disease.Journal of the American Heart Association · 2024Article
- Role of the kisspeptin-KISS1R axis in the pathogenesis of chronic kidney disease and uremic cardiomyopathy.GeroScience · 2024Article
- Chronic kidney disease may evoke anxiety by altering CRH expression in the amygdala and tryptophan metabolism in rats.Pflugers Archiv : European journal of physiology · 2024Article
- Neuregulin-1β Improves Uremic Cardiomyopathy and Renal Dysfunction in Rats.JACC. Basic to translational science · 2023Article
- The kisspeptin-1 receptor antagonist peptide-234 aggravates uremic cardiomyopathy in a rat model.Scientific reports · 2023Article
- miRNAs in Uremic Cardiomyopathy: A Comprehensive Review.International journal of molecular sciences · 2023Review
- Advances in the study of miRNAs in chronic kidney disease with cardiovascular complications.Frontiers in physiology · 2023Review
- Non-coding RNAs in the pathophysiology of heart failure with preserved ejection fraction.Frontiers in cardiovascular medicine · 2023Review
- Pathomechanism of oxidative stress in cardiovascularrenal remodeling and therapeutic strategies.Kidney research and clinical practice · 2022Article
- Review
- Investigation of the Antiremodeling Effects of Losartan, Mirabegron and Their Combination on the Development of Doxorubicin-Induced Chronic Cardiotoxicity in a Rat Model.International journal of molecular sciences · 2022Article
- Investigation of the Antihypertrophic and Antifibrotic Effects of Losartan in a Rat Model of Radiation-Induced Heart Disease.International journal of molecular sciences · 2021Article
- Ischemic preconditioning protects the heart against ischemia-reperfusion injury in chronic kidney disease in both males and females.Biology of sex differences · 2021Article
- Comparison of the antiremodeling effects of losartan and mirabegron in a rat model of uremic cardiomyopathy.Scientific reports · 2021Article
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Authors and funding
21 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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. Thus, the molecular mechanism of the development of LVH in CKD seems to be independent of the FOXO3, ERK1/2, AMPK, and AKT/mTOR-mediated pathways indicating unique features in this form of LVH.
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