Cardiac biomarkers in children with congenital heart disease

Sugimoto, Masaya; Kuwata, Seiko; Kurishima, Clara; Kim, Jeong Hye; Iwamoto, Yoich; Senzaki, Hideaki

doi:10.1007/s12519-015-0039-x

Cited by 51 publications

(40 citation statements)

References 58 publications

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“…Therapeutic blocking of miR-15 family members using LNA-modified anti-miRs after MI led to a reduction of infarct size, cardiac remodeling and enhanced cardiac function which corresponded with a decrease in cardiac fibrosis (102). Since many CHD patients present specific hemodynamic abnormalities, including left or RV volume overload and pulmonary hypertension as a conceivable consequence for instance of large VSDs, a resulting activation of fibroblasts may occur which in turn could facilitate cardiac fibrosis (103).…”

Section: Regulation Of Fibrosismentioning

confidence: 99%

MicroRNAs: pleiotropic players in congenital heart disease and regeneration

et al. 2017

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Congenital heart disease (CHD) is the leading cause of infant death, affecting approximately 4-14 live births per 1,000. Although surgical techniques and interventions have improved significantly, a large number of infants still face poor clinical outcomes. MicroRNAs (miRs) are known to coordinately regulate cardiac development and stimulate pathological processes in the heart, including fibrosis or hypertrophy and impair angiogenesis. Dysregulation of these regulators could therefore contribute (I) to the initial development of CHD and (II) at least partially to the observed clinical outcomes of many CHD patients by stimulating the aforementioned pathways. Thus, miRs may exhibit great potential as therapeutic targets in regenerative medicine. In this review we provide an overview of miR function and elucidate their role in selected CHDs, including hypoplastic left heart syndrome (HLHS), tetralogy of Fallot (TOF), ventricular septal defects (VSDs) and Holt-Oram syndrome (HOS). We then bridge this knowledge to the potential usefulness of miRs and/or their targets in therapeutic strategies for regenerative purposes in CHDs.

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Section: Regulation Of Fibrosismentioning

confidence: 99%

MicroRNAs: pleiotropic players in congenital heart disease and regeneration

et al. 2017

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“…Cardiac biomarkers facilitate the prediction of pathological changes that could provide information about the stress placed on the myocardial cells, the severity of the damage, the responses of neuro humoral factors, and the remodeling of the ventricle (Table 2). Moreover, assessment of cardiac biomarkers at an earlier stage can reduce the myocardial damage and severity of heart failure [11]. Therefore, children with CHD need most appropriate and delicate care [12] (Table 2).…”

Section: Hemodynamic or Cardiac Biomarkers Or Blood Biomarkersmentioning

confidence: 99%

Emerging Biomarkers of Congenital Heart Diseases and Disorders

Upadhyay

2016

JSRT

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Present review aims to discuss new emerging biomarkers that could facilitate authentic and fast diagnosis of congenital heart diseases. The population of congenital heart disease patients is increasing regularly and serious complications in adults are also enormously exceeding in comparison to children. Most of these congenital defects are un-curable and becoming challenging to treat. However, for predicting the prognosis of patient's different types of biomarkers i.e. hemodynamic, physiological, genetic, molecular, immunological, clinical and therapeutic biomarkers are explained. For sequential assessment of major structural and functional defects in CHD (congenital heart diseases) patients various bioassays and scientific methods are used to integrate defects with symptoms to find therapeutic decisions, targets and goals. This article tries to explore therapeutic options and solutions of CHD on the basis of emerging biomarkers and assess the need to advent new potential authentic biomarkers.

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“…While CHD mortality rates have been dramatically reduced in recent years thanks to advances in surgical practice and interventional technologies 1,3 , CHD patients continue to be at an increased risk of developing heart failure at a much younger age than the general population 4 . Despite early indicators of success, heart failure continues to take the lives of young children with CHD: 10 to 25% of newborns with a critical heart defect do not survive the first year, and 44% do not survive to 18 years of age 5,6 This unfortunate trend points to cardiac deficiencies in CHD that are not yet understood 7 .…”

Section: Introductionmentioning

confidence: 99%

Multiscale cardiac imaging to capture the whole heart and its internal cellular architecture, with applications to congenital heart disease

Rykiel

López

McQuiston

et al. 2020

Preprint

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9Efficient cardiac pumping depends on the morphological structure of the heart, but also on its 10 sub-cellular (ultrastructural) architecture, which enables cardiac contraction. In cases of 11 congenital heart defects, localized sub-cellular disruptions in architecture that increase the risk 12 of heart failure are only starting to be discovered. This is in part due to a lack of technologies 13 that can image the three dimensional (3D) heart structure, assessing malformations; and its 14 ultrastructure, assessing disruptions. We present here a multiscale, correlative imaging 15 procedure that achieves high-resolution images of the whole heart, using 3D micro-computed 16 tomography (micro-CT); and its ultrastructure, using 3D scanning electron microscopy (SEM). 17This combination of technologies has not been possible before in imaging the same cardiac 18 sample due to the heart large size, even when studying small fetal and neonatal animal models 19 (~5x5x5mm 3 ). Here, we achieved uniform fixation and staining of the whole heart, without losing 20 ultrastructural preservation (at the nm resolution range). Our approach enables multiscale 21 studies of cardiac architecture in models of congenital heart disease and beyond. 22 23 51 whole heart morphology and its sub-cellular organization (ultrastructural architecture). Our 52 multiscale procedure uses micro computed tomography (micro-CT) imaging to capture heart 53 morphology at micrometer resolution, and scanning electron microscopy (SEM) to capture 54 cardiac tissue ultrastructure at nanometer resolution. Current SEM technologies allow for three-55 dimensional (3D) imaging of sub-cellular architecture, enabling reconstruction and quantification 56 of ultrastructural features within a tissue volume 14-16 . Among 3D SEM methods, we have 57 selected serial block-face SEM (SBF-SEM) for ultrastructural imaging, as it allows 3D imaging of 58 relatively large volumes (sample size 40x60x40 µm 3 ). The methodology we present herein 59 improves upon previous protocols by achieving uniform staining of a relatively large heart 60 sample (3-4 mm wide, 5-6 mm long), circumventing micro-CT x-ray penetration issues, and 61 allowing sample screening and selection prior to full sample preparation. Our multiscale imaging, 62 further, enables mapping of structural and ultrastructural heart features. 63 129 thickening and enlargement of the RV wall. RV hypertrophy in TOF, however, develops over 130 time as the stenosis of the pulmonary artery increases pressure in the RV after birth 17 and was 131 not present in the heart examined in this study (see Figure 3 for a comparison of the selected 132 normal and TOF hearts). The TOF heart analyzed here featured supravalvular pulmonary 133 stenosis, a ventricular septal defect, and an overriding aorta. The right ventricle was enlarged 134and thin-walled compared to the control heart (Figure 3). Further, the TOF heart was missing 135 the right branch of the pulmonary artery. In humans, this rare condition, called unilateral 136

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Cardiac biomarkers in children with congenital heart disease

Cited by 51 publications

References 58 publications

MicroRNAs: pleiotropic players in congenital heart disease and regeneration

MicroRNAs: pleiotropic players in congenital heart disease and regeneration

Emerging Biomarkers of Congenital Heart Diseases and Disorders

Multiscale cardiac imaging to capture the whole heart and its internal cellular architecture, with applications to congenital heart disease

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