keyword
MENU ▼
Read by QxMD icon Read
search

heart remodelling

keyword
https://www.readbyqxmd.com/read/29353241/inhibition-of-endothelial-notch-signaling-impairs-fatty-acid-transport-and-leads-to-metabolic-and-vascular-remodeling-of-the-adult-heart
#1
Markus Jabs, Adam J Rose, Lorenz H Lehmann, Jacqueline Taylor, Iris Moll, Tjeerd P Sijmonsma, Stefanie E Herberich, Sven W Sauer, Gernot Poschet, Giuseppina Federico, Carolin Mogler, Eva-Maria Weis, Hellmut G Augustin, Minhong Yan, Norbert Gretz, Roland M Schmid, Ralf H Adams, Hermann-Joseph Gröne, Rüdiger Hell, Jürgen G Okun, Johannes Backs, Peter P Nawroth, Stephan Herzig, Andreas Fischer
Background -Nutrients are transported through endothelial cells before being metabolized in muscle cells. However, little is known about the regulation of endothelial transport processes. Notch signaling is a critical regulator of metabolism and angiogenesis during development. Here, we studied how genetic and pharmacological manipulation of endothelial Notch signaling in adult mice affects endothelial fatty acid transport, cardiac angiogenesis, and heart function. Methods -Endothelial-specific Notch inhibition was achieved by conditional genetic inactivation of Rbp-jκ in adult mice to analyze fatty acid metabolism and heart function...
January 20, 2018: Circulation
https://www.readbyqxmd.com/read/29352179/growth-and-remodeling-play-opposing-roles-during-postnatal-human-heart-valve-development
#2
Pim J A Oomen, Maria A Holland, Carlijn V C Bouten, Ellen Kuhl, Sandra Loerakker
Tissue growth and remodeling are known to govern mechanical homeostasis in biological tissue, but their relative contributions to homeostasis remain unclear. Here, we use mechanical models, fueled by experimental findings, to demonstrate that growth and remodeling have different effects on heart valve stretch homeostasis during physiological postnatal development. Two developmental stages were considered: early-stage (from infant to adolescent) and late-stage (from adolescent to adult) development. Our models indicated that growth and remodeling play opposing roles in preserving tissue stretch and with time...
January 19, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29352041/stress-signaling-jnk2-crosstalk-with-camkii-underlies-enhanced-atrial-arrhythmogenesis
#3
Jiajie Yan, Weiwei Zhao, Justin K Thomson, Xianlong Gao, Dominic M DeMarco, Elena Carrillo, Biyi Chen, Xiaomin Wu, Kenneth S Ginsburg, Mamdouh Bakhos, Donald M Bers, Mark E Anderson, Long-Sheng Song, Michael Fill, Xun Ai
Rationale: Atrial fibrillation (AF) is the most common arrhythmia and advanced age is an inevitable and predominant AF risk factor. However, the mechanisms that couple aging and AF propensity remain unclear, making targeted therapeutic interventions unattainable. Objective: To explore the functional role of an important stress-response c-Jun N-terminal kinase (JNK) in sarcoplasmic reticulum (SR) Ca2+ handling and consequently Ca2+-mediated atrial arrhythmias. Methods and Results: We employed a series of cutting-edge electrophysiological and molecular techniques, exploited the power of transgenic mouse models to detail the molecular mechanism, and verified its clinical applicability in parallel studies on donor human hearts...
January 19, 2018: Circulation Research
https://www.readbyqxmd.com/read/29351465/emerging-potential-benefits-of-modulating-nad-metabolism-in-cardiovascular-disease
#4
Daniel S Matasic, Charles Brenner, Barry London
Nicotinamide adenine dinucleotide (NAD+) and related metabolites are central mediators of fuel oxidation and bioenergetics within cardiomyocytes. Additionally, NAD+ is required for the activity of multifunctional enzymes including sirtuins and poly(ADP-ribose) polymerases (PARPs) that regulate post-translational modifications, DNA damage responses, and calcium signaling. Recent research indicates that NAD+ participates in a multitude of processes dysregulated in cardiovascular diseases. Therefore, supplementation of NAD+ precursors including nicotinamide riboside (NR) that boost or replete the NAD+ metabolome may be cardioprotective...
December 22, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29350681/aav-9-mediated-phosphatase-1-inhibitor-1-overexpression-improves-cardiac-contractility-in-unchallenged-mice-but-is-deleterious-in-pressure-overload
#5
D M Schwab, L Tilemann, R Bauer, M Heckmann, A Jungmann, M Wagner, J Burgis, C Vettel, H A Katus, A El-Armouche, O J Müller
The downregulation of β-adrenergic receptors (β-AR) and decreased cAMP-dependent protein kinase activity in failing hearts results in decreased phosphorylation and inactivation of phosphatase-inhibitor-1 (I-1), a distal amplifier element of β-adrenergic signaling, leading to increased protein phosphatase 1 activity and dephosphorylation of key phosphoproteins, including phospholamban. Downregulated and hypophosphorylated I-1 likely contributes to β-AR desensitization; therefore its modulation is a promising approach in heart failure treatment...
January 19, 2018: Gene Therapy
https://www.readbyqxmd.com/read/29349588/amphiregulin-enhances-cardiac-fibrosis-and-aggravates-cardiac-dysfunction-in-mice-with-experimental-myocardial-infarction-partly-through-activating-egfr-dependent-pathway
#6
Liang Liu, Xian Jin, Cui-Fen Hu, Ya-Ping Zhang, Zhong'e Zhou, Rong Li, Cheng-Xing Shen
Cardiac fibrosis (CF), a main process of ventricular remodeling after myocardial infarction (MI), plays a crucial role in the pathogenesis of heart failure (HF) post-MI. It is known that amphiregulin (AR) is involved in fibrosis of several organs. However, the expression of AR and its role post-MI are yet to be determined. This study aimed to investigate the impact of AR on CF post-MI and related mechanisms. Significantly upregulated AR expression was evidenced in the infarct border zone of MI mice in vivo and the AR secretion was enhanced in macrophages, but not in cardiac fibroblasts...
January 18, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29348018/myocardial-inflammation-predicts-remodeling-and-neuroinflammation-after-myocardial-infarction
#7
James T Thackeray, Henri C Hupe, Yong Wang, Jens P Bankstahl, Georg Berding, Tobias L Ross, Johann Bauersachs, Kai C Wollert, Frank M Bengel
BACKGROUND: The local inflammatory tissue response after acute myocardial infarction (MI) determines subsequent healing. Systemic interaction may induce neuroinflammation as a precursor to neurodegeneration. OBJECTIVES: This study sought to assess the influence of MI on cardiac and brain inflammation using noninvasive positron emission tomography (PET) of the heart-brain axis. METHODS: After coronary artery ligation or sham surgery, mice (n = 49) underwent serial whole-body PET imaging of the mitochondrial translocator protein (TSPO) as a marker of activated macrophages and microglia...
January 23, 2018: Journal of the American College of Cardiology
https://www.readbyqxmd.com/read/29346407/relaxin-reverses-inflammatory-and-immune-signals-in-aged-hearts
#8
Brian Martin, Beth Ann Gabris-Weber, Rajiv Reddy, Guillermo Romero, Ansuman Chattopadhyay, Guy Salama
BACKGROUND: 'Healthy' aging drives structural and functional changes in the heart including maladaptive electrical remodeling, fibrosis and inflammation, which lower the threshold for cardiovascular diseases such as heart failure (HF) and atrial fibrillation (AF). Despite mixed results in recent clinical trials, Relaxin-therapy for 2-days could reduce mortality by 37% at 180-days post-treatment, in patients with acute decompensated HF. Relaxin's short life-span (hours) but long-lasting protective actions led us to test the hypothesis that relaxin acts at a genomic level to reverse maladaptive remodeling in aging and HF...
2018: PloS One
https://www.readbyqxmd.com/read/29345195/mitochondrial-dysfunction-and-pulmonary-hypertension-cause-effect-or-both
#9
Jeffrey D Marshall, Isabel Bazan, Yi Zhang, Wassim H Fares, Patty J Lee
Pulmonary hypertension describes a heterogeneous disease defined by increased pulmonary artery pressures, and progressive increase in pulmonary vascular resistance due to pathologic remodeling of the pulmonary vasculature involving pulmonary endothelial cells, pericytes, and smooth muscle cells.  This process occurs under various conditions, and though these populations vary, the clinical manifestations are the same: progressive dyspnea, increases in right ventricular (RV) afterload and dysfunction, RV-pulmonary artery uncoupling, and right-sided heart failure with systemic circulatory collapse...
January 18, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29344827/molecular-imaging-of-cardiac-remodelling-after-myocardial-infarction
#10
REVIEW
Daniel Curley, Begoña Lavin Plaza, Ajay M Shah, René M Botnar
Myocardial infarction and subsequent heart failure is a major health burden associated with significant mortality and morbidity in western societies. The ability of cardiac tissue to recover after myocardial infarction is affected by numerous complex cellular and molecular pathways. Unbalance or failure of these pathways can lead to adverse remodelling of the heart and poor prognosis. Current clinical cardiac imaging modalities assess anatomy, perfusion, function, and viability of the myocardium, yet do not offer any insight into the specific molecular pathways involved in the repair process...
January 17, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29344374/cardioprotection-by-an-anti-masp-2-antibody-in-a-murine-model-of-myocardial-infarction
#11
James E Clark, Thomas Dudler, Michael S Marber, Wilhelm Schwaeble
Background: Myocardial ischaemia-reperfusion injury is a major cause of mortality and morbidity in the developed world. Many approaches have been investigated to counteract the pathological consequences associated with acute myocardial infarction (AMI) and cardiac remodelling. It is accepted that inflammation, and therefore activation of the complement pathway, is a crucial step in the pathogenesis of this injury, and many attempts have been made to ameliorate the infarction and consequent dysfunction using anticomplement therapy, with mixed success...
2018: Open Heart
https://www.readbyqxmd.com/read/29342503/the-molecular-basis-for-dysregulated-activation-of-nkx2-5-in-vascular-remodelling-of-systemic-sclerosis
#12
Athina Dritsoula, Ioannis Papaioannou, Sandra G Guerra, Carmen Fonseca, Javier Martin, Ariane L Herrick, David J Abraham, Christopher P Denton, Markella Ponticos
OBJECTIVE: NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling. In this study, we sought to investigate mechanisms that activate NKX2-5 expression in diseased vessels, such as scleroderma associated pulmonary hypertension (SSc-PH), and identify genetic variability that potentially underlies susceptibility to specific vascular complications...
January 17, 2018: Arthritis & Rheumatology
https://www.readbyqxmd.com/read/29341932/synthetic-extracellular-matrix-mimic-hydrogel-improves-efficacy-of-mesenchymal-stromal-cell-therapy-for-ischemic-cardiomyopathy
#13
Maria Chiara Ciuffreda, Giuseppe Malpasso, Cindy Chokoza, Deon Bezuidenhout, Kyle P Goetsch, Manuela Mura, Federica Pisano, Neil H Davies, Massimiliano Gnecchi
BACKGROUND: Mesenchymal stromal cells (MSC) repair infarcted hearts mainly through paracrine mechanisms. Low cell engraftment limits the release of soluble paracrine factors (SF) over time and, consequently, MSC efficacy. We tested whether a synthetic extracellular matrix mimic, a hydrogel containing heparin (H-HG), could ameliorate MSC engraftment and binding/release of SF, thus improving MSC therapy efficacy. METHODS AND RESULTS: In vitro, rat bone-marrow MSC (rBM-MSC) were seeded and grown into H-HG...
January 13, 2018: Acta Biomaterialia
https://www.readbyqxmd.com/read/29338868/survival-and-reoperation-pattern-after-20%C3%A2-years-of-experience-with-aortic-valve-sparing-root-replacement-in-patients-with-tricuspid-and-bicuspid-valves
#14
Stefan Klotz, Sina Stock, Hans-Hinrich Sievers, Michael Diwoky, Michael Petersen, Ulrich Stierle, Doreen Richardt
OBJECTIVE: Remodeling or reimplantation are established operative techniques of aortic valve-sparing root replacement. Long-term follow-up is necessary comparing tricuspid and bicuspid aortic valves. METHODS: A total of 315 patients (tricuspid, n = 225, bicuspid, n = 89, quadricuspid, n = 1; remodeling, n = 101, reimplantation, n = 214) were evaluated. Mean follow-up was 10.1 ± 5.6 and 6.4 ± 4.2 years for the remodeling and reimplantation group, respectively...
December 13, 2017: Journal of Thoracic and Cardiovascular Surgery
https://www.readbyqxmd.com/read/29337094/vitamin-d-attenuates-pressure-overload-induced-cardiac-remodeling-and-dysfunction-in-mice
#15
Liang Zhang, Xiao Yan, Jie Bai, Tesfaldet Habtemariam Hidru, Qing-Shan Wang, Hui-Hua Li
Vitamin D (VD) and its analogues play critical roles in metabolic and cardiovascular diseases. Recent studies have demonstrated that VD exerts a protective role in cardiovascular diseases. However, the beneficial effect of VD on pressure overload-induced cardiac remodeling and dysfunction and its underlying mechanisms are not fully elucidated. In this study, cardiac dysfunction and hypertrophic remodeling in mice were induced by pressure overload. Cardiac function was evaluated by echocardiography, and myocardial histology was detected by H&E and Masson's trichrome staining...
January 11, 2018: Journal of Steroid Biochemistry and Molecular Biology
https://www.readbyqxmd.com/read/29337052/sweet-yet-underappreciated-proteoglycans-and-extracellular-matrix-remodeling-in-heart-disease
#16
REVIEW
Geir Christensen, Kate M Herum, Ida G Lunde
Extracellular matrix remodeling is extensive in several heart diseases and hampers cardiac filling, often leading to heart failure. Proteoglycans have over the last two decades emerged as molecules with important roles in matrix remodeling and fibrosis in the heart. Here we discuss and review current literature on proteoglycans that have been studied in cardiac remodeling. The small leucine rich proteoglycans (SLRPs) are located within the extracellular matrix and are organizers of the matrix structure. Membrane-bound proteoglycans, such as syndecans and glypicans, act as receptors and direct cardiac fibroblast signaling...
January 11, 2018: Matrix Biology: Journal of the International Society for Matrix Biology
https://www.readbyqxmd.com/read/29335891/serum-bilirubin-concentration-is-associated-with-left-ventricular-remodeling-in-patients-with-type-2-diabetes-mellitus-a-cohort-study
#17
Tomoaki Inoue, Noriyuki Sonoda, Shinsuke Hiramatsu, Shinichiro Kimura, Yoshihiro Ogawa, Toyoshi Inoguchi
INTRODUCTION: Previous studies have shown that serum bilirubin concentration is inversely associated with the risk of cardiovascular disease. The relationship between serum bilirubin concentration and left ventricular geometry, however, has not been investigated in patients with diabetes mellitus. METHODS: In this cohort study, 158 asymptomatic patients with type 2 diabetes mellitus without overt heart disease were enrolled. Left ventricular structure and function were assessed using echocardiography...
January 15, 2018: Diabetes Therapy: Research, Treatment and Education of Diabetes and related Disorders
https://www.readbyqxmd.com/read/29335616/roles-of-angiotensin-ii-type-2-receptor-in-mice-with-fetal-growth-restriction
#18
Toshifumi Yamauchi, Masaki Mogi, Harumi Kan-No, Bao-Shuai Shan, Akinori Higaki, Li-Juan Min, Takashi Higaki, Jun Iwanami, Ei-Ichi Ishii, Masatsugu Horiuchi
Our previous report indicated that vascular injury enhances vascular remodeling in fetal growth restriction (FGR) mice. The angiotensin II type 2 receptor (AT2R) is relatively highly expressed in fetal mice. Therefore, we investigated the roles of AT2R in FGR-induced cardiovascular disease using AT2R knockout (AT2KO) mice. Dams (wild-type and AT2KO mice) were fed an isocaloric diet containing 20% protein (NP) or 8% protein (LP) until delivery. Arterial blood pressure, body weight, and histological changes in organs were investigated in offspring...
January 15, 2018: Hypertension Research: Official Journal of the Japanese Society of Hypertension
https://www.readbyqxmd.com/read/29334670/genetic-ablation-of-trpv1-exacerbates-pressure-overload-induced-cardiac-hypertrophy
#19
Beihua Zhong, Jack Rubinstein, Shuangtao Ma, Donna H Wang
Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses...
January 12, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29333636/in-search-of-markers-of-pulmonary-vascular-remodelling-in-pulmonary-hypertension-due-to-left-heart-disease
#20
EDITORIAL
Emmanouil Tampakakis
No abstract text is available yet for this article.
January 15, 2018: European Journal of Heart Failure
keyword
keyword
111827
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"