Functional Screening Identifies MicroRNAs as Multi-Cellular Regulators of Heart Failure

Verjans, Robin; Derks, Wouter; Korn, Kerstin; Sönnichsen, Birte; Leeuwen, R.E.W. van; Schroen, Blanche; Bilsen, Marc van; Heymans, Stéphane

doi:10.1038/s41598-019-41491-9

Cited by 28 publications

(17 citation statements)

References 67 publications

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“…There are a number of reports on miRNAs that regulate accumulation of extracellular matrix in the heart during aging or in response to injury, such as miR-125b, miR-29, miR-21, miR-18/19 [62][63][64][65][66]. MiR-125b has been shown to play an essential role in regulating cardiac fibrosis partially via silencing multiple anti-fibrotic elements, including p53 and apelin.…”

Section: Cardiac Senescencementioning

confidence: 99%

Regulatory Mechanisms of Mitochondrial Function and Cardiac Aging

Lin

Kerkelä

2020

IJMS

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Aging is a major risk factor for cardiovascular diseases (CVDs), the major cause of death worldwide. Cardiac myocytes, which hold the most abundant mitochondrial population, are terminally differentiated cells with diminished regenerative capacity in the adult. Cardiomyocyte mitochondrial dysfunction is a characteristic feature of the aging heart and one out of the nine features of cellular aging. Aging and cardiac pathologies are also associated with increased senescence in the heart. However, the cause and consequences of cardiac senescence during aging or in cardiac pathologies are mostly unrecognized. Further, despite recent advancement in anti-senescence therapy, the targeted cell type and the effect on cardiac structure and function have been largely overlooked. The unique cellular composition of the heart, and especially the functional properties of cardiomyocytes, need to be considered when designing therapeutics to target cardiac aging. Here we review recent findings regarding key factors regulating cell senescence, mitochondrial health as well as cardiomyocyte rejuvenation.

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Section: Cardiac Senescencementioning

confidence: 99%

Regulatory Mechanisms of Mitochondrial Function and Cardiac Aging

Lin

Kerkelä

2020

IJMS

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“…In addition, miR-223-3p could also accelerate heart failure depending on its pro-inflammatory effects in macrophages including activation and polarization of macrophage toward a pro-inflammatory (M1) phenotype, as well as induction of inflammation markers and secretion of cytokines, probably contributing to the development of heart failure (122,123,144).…”

Section: Effect Of Mir-223-3p On Pathophysiological Processes In Hearmentioning

confidence: 99%

MiR-223-3p in Cardiovascular Diseases: A Biomarker and Potential Therapeutic Target

Zhang

Shen

Shi

et al. 2021

Front. Cardiovasc. Med.

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Cardiovascular diseases, involving vasculopathy, cardiac dysfunction, or circulatory disturbance, have become the major cause of death globally and brought heavy social burdens. The complexity and diversity of the pathogenic factors add difficulties to diagnosis and treatment, as well as lead to poor prognosis of these diseases. MicroRNAs are short non-coding RNAs to modulate gene expression through directly binding to the 3′-untranslated regions of mRNAs of target genes and thereby to downregulate the protein levels post-transcriptionally. The multiple regulatory effects of microRNAs have been investigated extensively in cardiovascular diseases. MiR-223-3p, expressed in multiple cells such as macrophages, platelets, hepatocytes, and cardiomyocytes to modulate their cellular activities through targeting a variety of genes, is involved in the pathological progression of many cardiovascular diseases. It participates in regulation of several crucial signaling pathways such as phosphatidylinositol 3-kinase/protein kinase B, insulin-like growth factor 1, nuclear factor kappa B, mitogen-activated protein kinase, NOD-like receptor family pyrin domain containing 3 inflammasome, and ribosomal protein S6 kinase B1/hypoxia inducible factor 1 α pathways to affect cell proliferation, migration, apoptosis, hypertrophy, and polarization, as well as electrophysiology, resulting in dysfunction of cardiovascular system. Here, in this review, we will discuss the role of miR-223-3p in cardiovascular diseases, involving its verified targets, influenced signaling pathways, and regulation of cell function. In addition, the potential of miR-223-3p as therapeutic target and biomarker for diagnosis and prediction of cardiovascular diseases will be further discussed, providing clues for clinicians.

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“…Although there is a large body of evidence regarding up-and downregulation of genes for potassium channels, SERCA, subunits of receptors, signal molecules, proinflammatory cytokines, apoptotic mediators (Bax, caspase-9) in myocardium [213][214][215][216], and miRNAs are considered rather targets for personifying intervention and translational therapy, as well as prognosticators than diagnostic biomarkers for adverse cardiac remodelling and HF [217]. However, having signatures of miRNAs, which correspond to adverse cardiac remodelling, HF, sudden death, and cardiac abnormalities with established poor prognosis, such as concentric LV hypertrophy, fibrosis, and inflammation, it has not completely understood whether the "miRNA card" personally created for each patient will have clinical significance in the prediction of HF [33,218].…”

Section: Other Biomarkers Of Cardiac Remodellingmentioning

confidence: 99%

Adverse Cardiac Remodelling after Acute Myocardial Infarction: Old and New Biomarkers

Berezin

2020

Disease Markers

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The prevalence of heart failure (HF) due to cardiac remodelling after acute myocardial infarction (AMI) does not decrease regardless of implementation of new technologies supporting opening culprit coronary artery and solving of ischemia-relating stenosis with primary percutaneous coronary intervention (PCI). Numerous studies have examined the diagnostic and prognostic potencies of circulating cardiac biomarkers in acute coronary syndrome/AMI and heart failure after AMI, and even fewer have depicted the utility of biomarkers in AMI patients undergoing primary PCI. Although complete revascularization at early period of acute coronary syndrome/AMI is an established factor for improved short-term and long-term prognosis and lowered risk of cardiovascular (CV) complications, late adverse cardiac remodelling may be a major risk factor for one-year mortality and postponded heart failure manifestation after PCI with subsequent blood flow resolving in culprit coronary artery. The aim of the review was to focus an attention on circulating biomarker as a promising tool to stratify AMI patients at high risk of poor cardiac recovery and developing HF after successful PCI. The main consideration affects biomarkers of inflammation, biomechanical myocardial stress, cardiac injury and necrosis, fibrosis, endothelial dysfunction, and vascular reparation. Clinical utilities and predictive modalities of natriuretic peptides, cardiac troponins, galectin 3, soluble suppressor tumorogenicity-2, high-sensitive C-reactive protein, growth differential factor-15, midregional proadrenomedullin, noncoding RNAs, and other biomarkers for adverse cardiac remodelling are discussed in the review.

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Functional Screening Identifies MicroRNAs as Multi-Cellular Regulators of Heart Failure

Cited by 28 publications

References 67 publications

Regulatory Mechanisms of Mitochondrial Function and Cardiac Aging

Regulatory Mechanisms of Mitochondrial Function and Cardiac Aging

MiR-223-3p in Cardiovascular Diseases: A Biomarker and Potential Therapeutic Target

Adverse Cardiac Remodelling after Acute Myocardial Infarction: Old and New Biomarkers

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