microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases

Lucia, Claudio de; Komici, Klara; Borghetti, Giulia; Femminella, Grazia Daniela; Bencivenga, Leonardo; Cannavò, Alessandro; Corbi, Graziamaria; Ferrara, Nicola; Houser, Steven R.; Koch, Walter J.; Rengo, Giuseppe

doi:10.3389/fmed.2017.00074

Cited by 81 publications

(57 citation statements)

References 260 publications

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“…We have also systematically adjusted for age, which is known to greatly influence the variations in the level of circulating miRNAs. (37)(38)(39)(40)(41) There may be several explanations for the discrepancies between the previously published studies and the present results. First, we systematically adjusted for age, which was not always performed in other studies.…”

Section: Discussioncontrasting

confidence: 99%

“…In addition, the association between miRNA serum levels and aging has been reported in several studies to date in a wide range of physiological processes. (37)(38)(39)(40)(41) For example, it has been established that miR-188 is a key regulator in the age-related switch between osteogenesis and adipogenesis in bone marrow mesenchymal stem cells. (42) Second, we may assume that the influence of the circulating miRNAs differs over the life course.…”

Section: Discussionmentioning

confidence: 99%

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Lack of Association Between Select Circulating miRNAs and Bone Mass, Turnover, and Fractures: Data From the OFELY Cohort

Feurer

Kan

Croset

et al. 2019

Journal of Bone and Mineral Research

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Postmenopausal osteoporosis is characterized by the occurrence of fragility fracture with an increase in morbidity and mortality. Recently, microRNAs (miRNAs) have raised interest as regulators of translational repression, mediating a number of key processes, including bone tissue in both physiological and diseased states. The aim of this study was to examine the serum levels of 32 preselected miRNAs with reported function in bone and their association with osteoporotic fracture. We performed cross-sectional and longitudinal analyses from the OFELY Cohort. Serum levels of the miRNAs were quantified by qRT-PCR in 682 women: 99 premenopausal and 583 postmenopausal women, with 1 and 122 women with prevalent fragility fractures in each group, respectively. We have collected clinical variables (such as age, prevalent, and incident fractures), bone turnover markers (BTMs), BMD by dual X-ray absorptiometry, and bone microarchitecture with HRpQCT. We observed a number of miRNAs to be associated with fragility fractures (prevalent or incident), BTMs, BMD, and microarchitecture. This effect, however, was negated after age adjustment. This may be because age was also strongly associated with the serum levels of the 32 miRNAs (correlation coefficient up to 0.49), confirming previous findings. In conclusion, in a well-characterized prospective cohort with a sizeable sample size, we found no evidence that these 32 preselected miRNAs were not associated with BTMs, BMD, microarchitecture, and or fragility fractures. Ã CTX, mg/L (min-max) 0.466 (0.057-1.470) 0.374 (0.107-1.030) 0.481 (0.057-1.470) Ã Osteocalcin, ng/mL (min-max) Ã Ã p value considered as significant if <0.05. Tt.vBMD ¼ total volumetric bone mineral density; Ct.vBMD ¼ cortical volumetric bone mineral density; Tb.vBMD ¼ trabecular volumetric bone mineral density; BAP ¼ bone alkaline phosphatase. Journal of Bone and Mineral Research LACK OF ASSOCIATION BETWEEN miRNAs AND BONE: DATA FROM THE OFELY COHORT 5 FEURER ET AL. Ã Radius Tt.vBMD, mg/cm 3 (min-max) 245.6 (122.9-482.1) 278.1 (101.9-515.8) Ã Radius Ct.vBMD, mg/cm 3 (min-max) 771.9 (556.9-956.4) 803.0 (572.6-1004.8) Ã Radius Tb.vBMD, mg/cm 3 (min-max) 123.2 (50.3-264.0) 141.8 (17.5-262.8) Ã Tibia Tt.vBMD, mg/cm 3 (min-max) 228.3 (124.2-371.2) 252.8 (109.0-417.4) Ã Tibia Ct.vBMD, mg/cm 3 (min-max) 702.6 (437.7-912.7) 744.6 (376.7-976.6) Ã Tibia Tb.vBMD, mg/cm 3 (min-max) 133.6 (52.0-212.6) 149.3 (31.9-254.7) Ã CTX, mg/L (min-max) 0.463 (0.057-1.16) 0.484 (0.062-1.470) NS Osteocalcin, ng/mL (min-max) 28.6 (4.2-90.2) 27.7 (6.5-86.2) NS P1NP, ng/mL (min-max) 49.0 (8.1-138.6) 21.5 (10.0-139.7) NS BAP, UI/L (min-max) 39.3 (15.2-69.4) 38.8 (10.1-88.6) NS Ã p-value considered as significant if <0.05. Tt.vBMD ¼ total volumetric bone mineral density; Ct.vBMD ¼ cortical volumetric bone mineral density; Tb.vBMD ¼ trabecular volumetric bone mineral density; BAP ¼ bone alkaline phosphatase. 8 FEURER ET AL.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Lack of Association Between Select Circulating miRNAs and Bone Mass, Turnover, and Fractures: Data From the OFELY Cohort

Feurer

Kan

Croset

et al. 2019

Journal of Bone and Mineral Research

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“…In the AF process, the effect of up-regulated MiR-328 has been demonstrated by reducing the density of the Ca 2+ channel type L. This contributed to atrial electrical remodeling. Overexpression of miR-328 has a pro-arrhythmogenic effect, confirmed in animal models and the delivery of the antagomiR was able to reverse the arrhythmogenic phenotype [83].…”

Section: Potential Of Mirnas As Treatment Of Afmentioning

confidence: 83%

“…Technologies used in miRNA therapies utilize lipid-based vehicles, various viral systems, biodegradable scaffolds, so-called "exosome-encapsulated" miRNAs, or light-induced antagomir activation [83].…”

Section: Potential Of Mirnas As Treatment Of Afmentioning

confidence: 99%

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Molecular Mechanisms, Diagnostic Aspects and Therapeutic Opportunities of Micro Ribonucleic Acids in Atrial Fibrillation

Böhm

Vachalcová²,

Snopek

et al. 2020

IJMS

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Micro ribonucleic acids (miRNAs) are short non-coding RNA molecules responsible for regulation of gene expression. They are involved in many pathophysiological processes of a wide spectrum of diseases. Recent studies showed their involvement in atrial fibrillation. They seem to become potential screening biomarkers for atrial fibrillation and even treatment targets for this arrhythmia. The aim of this review article was to summarize the latest knowledge about miRNA and their molecular relation to the pathophysiology, diagnosis and treatment of atrial fibrillation.

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MiR‐182‐5p inhibited oxidative stress and apoptosis triggered by oxidized low‐density lipoprotein via targeting toll‐like receptor 4

Qin

Peng

et al. 2018

Journal Cellular Physiology

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MicroRNAs (miRNAs) exhibit various roles in multiple biological processes and abnormal expression of miR-182-5p has been involved in many diseases. However, the role miR-182-5p in Atherosclerosis (AS) remains poorly understood. In our current investigation, an AS model was established by using oxidized low-density lipoprotein (ox-LDL) in RAW264.7 cells. miR-182-5p was markedly decreased in AS model dose-dependently and time-dependently. Additionally, CD36, oil-red staining levels, TC, and TG were inhibited by miR-182-5p mimics, meanwhile ROS levels, MDA, and cell apoptosis were also restrained with an enhancement of SOD activity. Consistently, opposite results were exhibited when miR-182-5p inhibitors were transfected into RAW264.7 cells. It is well known that toll-like receptor 4 (TLR4) is responsible for many inflammation diseases. By using bioinformatics analysis, TLR4 was indicated as a potential target of miR-182-5p. We observed TLR4 was activated in AS models and miR-182-5p could repress AS progression by targeting TLR4 in vitro. In conclusion, we uncovered that miR-182-5p played significant roles in AS through inhibiting oxidative stress and apoptosis via inactivating TLR4 expression.

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microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases

Cited by 81 publications

References 260 publications

Lack of Association Between Select Circulating miRNAs and Bone Mass, Turnover, and Fractures: Data From the OFELY Cohort

Lack of Association Between Select Circulating miRNAs and Bone Mass, Turnover, and Fractures: Data From the OFELY Cohort

Molecular Mechanisms, Diagnostic Aspects and Therapeutic Opportunities of Micro Ribonucleic Acids in Atrial Fibrillation

MiR‐182‐5p inhibited oxidative stress and apoptosis triggered by oxidized low‐density lipoprotein via targeting toll‐like receptor 4

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