Commentary: MicroRNA-221/222 Family Counteracts Myocardial Fibrosis in Pressure Overload-Induced Heart Failure

Schmitz, Boris; Brand, Stefan-Martin

doi:10.3389/fcvm.2018.00095

Cited by 2 publications

(1 citation statement)

References 14 publications

(18 reference statements)

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“…48) Meanwhile, miR-222-3p plays a role in cardiac hypertrophy and HF. 49) Increased expression of miR-223-3p in the LV of left coronary artery ligation-induced MI rats after surgery may predict the development of HF. In addition to these miRNAs, upregulation of miR-350 and downregulation of miR-9 were identified as being involved in cardiac hypertrophy in this study.…”

Section: Discussionmentioning

confidence: 99%

The Role of SGLT2 Inhibitor Ipragliflozin on Cardiac Hypertrophy and microRNA Expression Profiles in a Non-diabetic Rat Model of Cardiomyopathy

Takasu

2022

Biological & Pharmaceutical Bulletin

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Evidence from clinical trials suggests that the cardioprotective effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors may arise through non-glycemic control-related mechanisms. Further, the cardiovascular advantages of SGLT2 inhibitors are likely present among non-diabetic patients with known cardiovascular diseases (CVDs). Here, we studied the impact of ipragliflozin, a selective SGLT2 inhibitor, on cardiac histopathology and microRNA (miRNA) expression profiles in a non-diabetic rat model of cardiomyopathy. Ipragliflozin was added to chow (0.01% (w/w)) and given to male DahlS.Z-Lepr fa /Lepr fa (DS/obese) rats for 6 weeks. Similarly aged male DahlS.Z-Lepr /Lepr (DS/lean) rats were treated as controls. Measurements of systolic blood pressure (SBP) and heart rate (HR) were taken every other week. Following ipragliflozin treatment for 6 weeks, we conducted echocardiography, histopathological examination, and miRNA expression analysis (microarray). The impact of ipragliflozin on blood parameters was additionally examined. In DS/obese rats, ipragliflozin reduced SBP without affecting HR, reduced interventricular septal thickness in echocardiography and left ventricular (LV) organ weight, and improved hypertrophy of cardiomyocytes according to histopathological experiments. Further, ipragliflozin reduced plasma inflammatory cytokine levels in DS/obese rats. Additionally, ipragliflozin treatment altered the expression profile of miRNAs related to cardiac hypertrophy and heart failure in the LV compared to DS/obese control rats. Ipragliflozin prevented LV hypertrophy and altered related miRNA expression profiles in non-diabetic DS/obese rats. These findings suggest that miRNAs may play a partial role in regulating the structure of the heart and that SGLT2 inhibitors may exert cardio-protective effects by changing miRNA expression profiles in non-diabetic patients with CVDs.

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Section: Discussionmentioning

confidence: 99%

The Role of SGLT2 Inhibitor Ipragliflozin on Cardiac Hypertrophy and microRNA Expression Profiles in a Non-diabetic Rat Model of Cardiomyopathy

Takasu

2022

Biological & Pharmaceutical Bulletin

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Influence of miR-221/222 on cardiomyocyte calcium handling and function

et al. 2021

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Background Cardiovascular disease is the leading cause of death worldwide. Cardiac electrical remodeling including altered ion channel expression and imbalance of calcium homeostasis can have detrimental effects on cardiac function. While it has been extensively reported that miR-221/222 are involved in structural remodeling, their role in electrical remodeling still has to be evaluated. We previously reported that subunits of the L-type Ca2+ channel (LTCC) are direct targets of miR-221/222. Furthermore, HL-1 cells transfected with miR-221 or -222 mimics showed a reduction in LTCC current density while the voltage-dependence of activation was not altered. The aim of the present study was to determine the influence of miR-221/222 on cardiomyocyte calcium handling and function. Results Transient transfection of HL-1 cells with miR-221/222 mimics led to slower depolarization-dependent Ca2+ entry and increased proportion of non-responding cells. Angiotensin II-induced Ca2+ release from the SR was not affected by miR-221/222. In miR-222-transfected neonatal cardiomyocytes the isoprenaline-induced positive inotropic effect on the intracellular Ca2+ transient was lost and the positive chronotropic effect on spontaneous beating activity was strongly reduced. This could have severe consequences for cardiomyocytes and could lead to a reduced contractility and systolic dysfunction of the whole heart. Conclusions This study adds a new role of miR-221/222 in cardiomyocytes by showing the impact on β-adrenergic regulation of LTCC function, calcium handling and beating frequency. Together with the previous report that miR-221/222 reduce GIRK1/4 function and LTCC current density, it expands our knowledge about the role of these miRs on cardiac ion channel regulation.

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Commentary: MicroRNA-221/222 Family Counteracts Myocardial Fibrosis in Pressure Overload-Induced Heart Failure

Cited by 2 publications

References 14 publications

The Role of SGLT2 Inhibitor Ipragliflozin on Cardiac Hypertrophy and microRNA Expression Profiles in a Non-diabetic Rat Model of Cardiomyopathy

The Role of SGLT2 Inhibitor Ipragliflozin on Cardiac Hypertrophy and microRNA Expression Profiles in a Non-diabetic Rat Model of Cardiomyopathy

Influence of miR-221/222 on cardiomyocyte calcium handling and function

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