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Cardiac development, cardiac remodelling, cardiac function

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https://www.readbyqxmd.com/read/29773058/non-cardiomyocytes-in-heart-regeneration
#1
Jie Feng, Yandong Li, Yu Nie
Heart failure represents a challenging clinical and public health problem and is associated with significant morbidity and mortality. Mechanistically, loss of cardiomyocytes leads to decompensated ventricular remodeling, which eventually progressed to cardiac failure. Regenerative medicine aimed to supplement functional cardiomyocytes is supposedly a promising approach for the effective treatment of heart failure. Over the past decades, investigations on heart regeneration have revealed the regulating networks of cardiomyocyte proliferation...
May 17, 2018: Current Drug Targets
https://www.readbyqxmd.com/read/29771311/pathobiology-of-cardiac-dyssynchrony-and-resynchronization-therapy
#2
Uyên Châu Nguyên, Nienke J Verzaal, Frans A van Nieuwenhoven, Kevin Vernooy, Frits W Prinzen
Synchronous ventricular electrical activation is a prerequisite for adequate left ventricular (LV) systolic function. Conduction abnormalities such as left bundle branch block, and ventricular pacing lead to a dyssynchronous electrical activation sequence, which may have deleterious consequences. The present review attempts to connect the various processes involved in the development of 'dyssynchronopathy', and its correction by cardiac resynchronization therapy (CRT). Abnormal electrical impulse conduction leads to abnormal contraction, characterized by regional differences in timing as well as shortening patterns and amount of external work performed...
May 15, 2018: Europace: European Pacing, Arrhythmias, and Cardiac Electrophysiology
https://www.readbyqxmd.com/read/29769710/jdp2-overexpression-provokes-cardiac-dysfunction-in-mice
#3
Jacqueline Heger, Julia Bornbaum, Alona Würfel, Christian Hill, Nils Brockmann, Renáta Gáspár, János Pálóczi, Zoltán V Varga, Márta Sárközy, Péter Bencsik, Tamás Csont, Szilvia Török, Baktybek Kojonazarov, Ralph Theo Schermuly, Kerstin Böngler, Mariana Parahuleva, Peter Ferdinandy, Rainer Schulz, Gerhild Euler
The transcriptional regulator JDP2 (Jun dimerization protein 2) has been identified as a prognostic marker for patients to develop heart failure after myocardial infarction. We now performed in vivo studies on JDP2-overexpressing mice, to clarify the impact of JDP2 on heart failure progression. Therefore, during birth up to the age of 4 weeks cardiac-specific JDP2 overexpression was prevented by doxycycline feeding in transgenic mice. Then, JDP2 overexpression was started. Already after 1 week, cardiac function, determined by echocardiography, decreased which was also resembled on the cardiomyocyte level...
May 16, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29767239/time%C3%A2-dependent-and-independent-effects-of-thyroid-hormone-administration-following-myocardial-infarction-in-rats
#4
Ioanna Iliopoulou, Iordanis Mourouzis, George I Lambrou, Dimitra Iliopoulou, Dimitrios-Dionysios Koutsouris, Constantinos Pantos
Cardiac function is reduced following myocardial infarction (MI) due to myocardial injury and alterations in the viable non‑ischemic myocardium, a process known as cardiac remodeling. The current treatments available for patients with acute MI (AMI) reduce infarct size, preserve left ventricular (LV) function and improve survival; however, these treatments do not prevent remodeling, which can lead to heart failure. The aim of the present study was to investigate the effects of thyroid hormone (TH) treatment following MI in an in vivo rat model...
May 11, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29764718/metabolic-syndrome-associates-with-left-atrial-dysfunction
#5
K Nyman, M Granér, M O Pentikäinen, J Lundbom, A Hakkarainen, R Sirén, M S Nieminen, M-R Taskinen, N Lundbom, K Lauerma
BACKGROUND AND AIMS: Obesity and metabolic syndrome (MetS) are risk factors of atrial fibrillation (AF), but limited data exist on their effect on left atrial (LA) function. The aim of the study was to evaluate the effects of cardiac, hepatic and intra-abdominal ectopic fat depots and cardiometabolic risk factors on LA function in non-diabetic male subjects. METHODS AND RESULTS: Myocardial and hepatic triglyceride contents were measured with 1.5T 1 H-magnetic resonance spectroscopy and LA and left ventricular function, visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), epicardial and pericardial fat by magnetic resonance imaging (MRI) in 33 men with MetS and 40 men without MetS...
February 21, 2018: Nutrition, Metabolism, and Cardiovascular Diseases: NMCD
https://www.readbyqxmd.com/read/29760744/mst1-regulates-post-infarction-cardiac-injury-through-the-jnk-drp1-mitochondrial-fission-pathway
#6
Xisong Wang, Qing Song
Background: Post-infarction cardiac injury is closely associated with cardiac remodeling and heart dysfunction. Mammalian STE20-like kinase 1 (Mst1), a regulator of cellular apoptosis, is involved in cardiac remodeling in post-infarction heart, but the mechanisms remain poorly defined. We aimed to explore the role of Mst1 in regulating chronic post-infarction cardiac injury, with a focus on mitochondrial homoeostasis. Methods: Wild-type (WT) and Mst1-knockout mice were as the cardiac myocardial infarction model...
2018: Cellular & Molecular Biology Letters
https://www.readbyqxmd.com/read/29755986/implications-of-cellular-aging-in-cardiac-reprogramming
#7
Fabiana Passaro, Gianluca Testa
Aging is characterized by a chronic functional decline of organ systems which leads to tissue dysfunction over time, representing a risk factor for diseases development, including cardiovascular. The aging process occurring in the cardiovascular system involves heart and vessels at molecular and cellular level, with subsequent structural modifications and functional impairment. Several modifications involved in the aging process can be ascribed to cellular senescence, a biological response that limits the proliferation of damaged cells...
2018: Frontiers in Cardiovascular Medicine
https://www.readbyqxmd.com/read/29755853/reg3%C3%AE-from-cardiomyocytes-regulated-macrophage-migration-proliferation-and-functional-skewing-in-experimental-autoimmune-myocarditis
#8
Shanshan Zhou, Han Jiang, Han Wang, Hongxiang Lu, Rong Chen, Huaxi Xu, Zhaoliang Su, Xiaoyi Shao
Macrophages play critical roles in inflammatory initiation, development, resolution and cardiac regeneration of myocarditis. However, Reg3β, as a member of regenerating family of proteins, contributes to dedifferentiation of injury cardiomyocytes as well as cardiac function remodeling. It remains unclear whether Reg3β was associated with macrophages reprogramming during autoimmune myocarditis. Our results showed that Reg3β could effectively recruit macrophages, promoted their proliferation and phagocytosis, and facilitated their polarized into M2 macrophages...
2018: American Journal of Clinical and Experimental Immunology
https://www.readbyqxmd.com/read/29754254/interplay-between-cardiac-transcription-factors-and-non-coding-rnas-in-predisposing-to-atrial-fibrillation
#9
REVIEW
Alexander T Mikhailov, Mario Torrado
There is growing evidence that putative gene regulatory networks including cardio-enriched transcription factors, such as PITX2, TBX5, ZFHX3, and SHOX2, and their effector/target genes along with downstream non-coding RNAs can play a potentially important role in the process of adaptive and maladaptive atrial rhythm remodeling. In turn, expression of atrial fibrillation-associated transcription factors is under the control of upstream regulatory non-coding RNAs. This review broadly explores gene regulatory mechanisms associated with susceptibility to atrial fibrillation-with key examples from both animal models and patients-within the context of both cardiac transcription factors and non-coding RNAs...
May 12, 2018: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/29753320/adverse-effects-of-hif1a-mutation-and-maternal-diabetes-on-the-offspring-heart
#10
Radka Cerychova, Romana Bohuslavova, Frantisek Papousek, David Sedmera, Pavel Abaffy, Vladimir Benes, Frantisek Kolar, Gabriela Pavlinkova
BACKGROUND: Epidemiological studies show that maternal diabetes predisposes offspring to cardiovascular and metabolic disorders. However, the precise mechanisms for the underlying penetrance and disease predisposition remain poorly understood. We examined whether hypoxia-inducible factor 1 alpha, in combination with exposure to a diabetic intrauterine environment, influences the function and molecular structure of the adult offspring heart. METHODS AND RESULTS: In a mouse model, we demonstrated that haploinsufficient (Hif1a+/- ) offspring from a diabetic pregnancy developed left ventricle dysfunction at 12 weeks of age, as manifested by decreased fractional shortening and structural remodeling of the myocardium...
May 12, 2018: Cardiovascular Diabetology
https://www.readbyqxmd.com/read/29747850/imaging-right-left-ventricular-interactions
#11
REVIEW
Mark K Friedberg
The impact of one ventricle on the adjacent ventricle plays a key role in cardiac function. Ventricular-ventricular interactions are based on the arrangement in-series of the circulation and common pericardium, interventricular septum, and myocardial tracts. Imaging, in particular echocardiography, plays a central role in characterizing these interactions through geometric indices, septal configuration and motion, Doppler flow, timing of events in the ventricles and alterations in strain, remodeling, and diastolic filling with altered loading of the contralateral ventricle...
May 2018: JACC. Cardiovascular Imaging
https://www.readbyqxmd.com/read/29731719/rhace2-therapy-modifies-bleomycin-induced-pulmonary-hypertension-via-rescue-of-vascular-remodeling
#12
Anandharajan Rathinasabapathy, Andrew J Bryant, Toshio Suzuki, Christy Moore, Sheila Shay, Santhi Gladson, James D West, Erica J Carrier
Background: Pulmonary hypertension (PH) is a progressive cardiovascular disease, characterized by endothelial and smooth muscle dysfunction and vascular remodeling, followed by right heart failure. Group III PH develops secondarily to chronic lung disease such as idiopathic pulmonary fibrosis (IPF), and both hastens and predicts mortality despite of all known pharmacological interventions. Thus, there is urgent need for development of newer treatment strategies. Objective: Angiotensin converting enzyme 2 (ACE2), a member of the renin angiotensin family, is therapeutically beneficial in animal models of pulmonary vascular diseases and is currently in human clinical trials for primary PH...
2018: Frontiers in Physiology
https://www.readbyqxmd.com/read/29729330/paraoxonase-2-prevents-the-development-of-heart-failure
#13
Wei Li, David Kennedy, Zhili Shao, Xi Wang, Andre Klaassen Kamdar, Malory Weber, Kayla Mislick, Kathryn Kiefer, Rommel Morales, Brendan Agatisa-Boyle, Diana M Shih, Srinivasa T Reddy, Christine S Moravec, W H Wilson Tang
BACKGROUND: Mitochondrial oxidation is a major source of reactive oxygen species (ROS) and mitochondrial dysfunction plays a central role in development of heart failure (HF). Paraoxonase 2 deficient (PON2-def) mitochondria are impaired in function. In this study, we tested whether PON2-def aggravates HF progression. METHODS AND RESULTS: Using qPCR, immunoblotting and lactonase activity assay, we demonstrate that PON2 activity was significantly decreased in failing hearts despite increased PON2 expression...
May 2, 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29723269/17%C3%AE-estradiol-and-or-estrogen-receptor-alpha-signaling-blocks-protein-phosphatase-1-mediated-iso-induced-cardiac-hypertrophy
#14
Hsin-Yuan Fang, Meng-Yu Hung, Yueh-Min Lin, Sudhir Pandey, Chia-Chien Chang, Kuan-Ho Lin, Chia-Yao Shen, Vijaya Padma Viswanadha, Wei-Wen Kuo, Chih-Yang Huang
Earlier studies have shown that estrogen possess protective function against the development of pathological cardiac hypertrophy. However, the molecular mechanisms of estrogens (E2) protective effect are poorly understood. Additionally, abnormal activation of β-adrenergic signaling have been implicated in the development of pathological cardiac remodeling. However, the role of serine/threonine protein phosphatase 1 (PP1) in pathological cardiac remodeling under the influence of β-adrenergic signaling have been sparsely investigated...
2018: PloS One
https://www.readbyqxmd.com/read/29723239/analysis-of-the-microrna-signature-in-left-atrium-from-patients-with-valvular-heart-disease-reveals-their-implications-in-atrial-fibrillation
#15
Rosa Doñate Puertas, Audrey Jalabert, Emmanuelle Meugnier, Vanessa Euthine, Philippe Chevalier, Sophie Rome
BACKGROUND: Among the potential factors which may contribute to the development and perpetuation of atrial fibrillation, dysregulation of miRNAs has been suggested. Thus in this study, we have quantified the basal expressions of 662 mature human miRNAs in left atrium (LA) from patients undergoing cardiac surgery for valve repair, suffering or not from atrial fibrillation (AF) by using TaqMan® Low Density arrays (v2.0). RESULTS: Among the 299 miRNAs expressed in all patients, 42 miRNAs had altered basal expressions in patients with AF...
2018: PloS One
https://www.readbyqxmd.com/read/29716898/load-dependent-changes-in-left-ventricular-structure-and-function-in-a-pathophysiologically-relevant-murine-model-of-reversible-heart-failure
#16
Carla J Weinheimer, Attila Kovacs, Sarah Evans, Scot J Matkovich, Philip M Barger, Douglas L Mann
BACKGROUND: To better understand reverse left ventricular (LV) remodeling, we developed a murine model wherein mice develop LV remodeling after transverse aortic constriction (TAC) and a small apical myocardial infarct (MI) and undergo reverse LV remodeling after removal of the aortic band. METHODS AND RESULTS: Mice studied were subjected to sham (n=6) surgery or TAC+MI (n=12). Two weeks post-TAC+MI, 1 group underwent debanding (referred to as heart failure debanding [HF-DB] mice; n=6), whereas the aortic band remained in a second group (heart failure [HF] group; n=6)...
May 2018: Circulation. Heart Failure
https://www.readbyqxmd.com/read/29695980/cardiac-remodeling-endothelial-cells-have-more-to-say-than-just-no
#17
REVIEW
Vincent F M Segers, Dirk L Brutsaert, Gilles W De Keulenaer
The heart is a highly structured organ consisting of different cell types, including myocytes, endothelial cells, fibroblasts, stem cells, and inflammatory cells. This pluricellularity provides the opportunity of intercellular communication within the organ, with subsequent optimization of its function. Intercellular cross-talk is indispensable during cardiac development, but also plays a substantial modulatory role in the normal and failing heart of adults. More specifically, factors secreted by cardiac microvascular endothelial cells modulate cardiac performance and either positively or negatively affect cardiac remodeling...
2018: Frontiers in Physiology
https://www.readbyqxmd.com/read/29687888/epigenetics-of-aberrant-cardiac-wound-healing
#18
Adam Russell-Hallinan, Chris J Watson, John A Baugh
Remodeling of cardiac tissue architecture is essential for normal organ development and maintaining homeostasis after injury. Injurious insults to the heart, such as hypertension and myocardial infarction, promote cellular responses including stimulation of resident inflammatory cells, activation of endothelial cells and recruitment of immune cells, hypertrophy of cardiomyocytes, and activation of fibroblasts. The physiological goal of this coordinated cellular response is to repair damaged tissue while maintaining or restoring cardiac contractile function...
March 26, 2018: Comprehensive Physiology
https://www.readbyqxmd.com/read/29678849/effects-of-adenovirus-mediated-vegf165-gene-therapy-on-myocardial-infarction
#19
Chao Wang, Boya Zhang, Yu Lin, Yang Dong
AIM: To evaluate the role of adenovirus-mediated transduction human VEGF isoform 165 via direct myocardial injection in rats with an occluded circumflex coronary artery, and the possible underlying mechanism. METHODS: Sprague-Dawley rats were induced myocardial infarction (MI) with ligation of the left coronary artery. Rats were randomly divided into 4 groups: 1) the sham group; 2) the MI group; 3) the NS (normal saline) group and 4) the VEGF group. Direct myocardial injection of 0...
March 2018: Annals of Clinical and Laboratory Science
https://www.readbyqxmd.com/read/29674714/mechanisms-of-physiological-and-pathological-cardiac-hypertrophy
#20
REVIEW
Michinari Nakamura, Junichi Sadoshima
Cardiomyocytes exit the cell cycle and become terminally differentiated soon after birth. Therefore, in the adult heart, instead of an increase in cardiomyocyte number, individual cardiomyocytes increase in size, and the heart develops hypertrophy to reduce ventricular wall stress and maintain function and efficiency in response to an increased workload. There are two types of hypertrophy: physiological and pathological. Hypertrophy initially develops as an adaptive response to physiological and pathological stimuli, but pathological hypertrophy generally progresses to heart failure...
April 19, 2018: Nature Reviews. Cardiology
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