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Cardiac development, cardiac remodelling, cardiac function

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https://www.readbyqxmd.com/read/28231509/a-single-injection-of-protein-loaded-coacervate-gel-significantly-improves-cardiac-function-post-infarction
#1
H K Awada, D W Long, Z Wang, M P Hwang, K Kim, Y Wang
After myocardial infarction (MI), the heart undergoes fibrotic pathological remodeling instead of repair and regeneration. With multiple pathologies developing after MI, treatment using several proteins is expected to address this range of pathologies more effectively than a single-agent therapy. A factorial design of experiments study guided us to combine three complementary factors in one injection: tissue inhibitor of metalloproteinases-3 (TIMP-3) was embedded in a fibrin gel for signaling in the initial phase of the treatment, while basic fibroblast growth factor (FGF-2) and stromal cell-derived factor 1-alpha (SDF-1α) were embedded in heparin-based coacervates for sustained release and distributed within the same fibrin gel to exert their effects over a longer period...
February 17, 2017: Biomaterials
https://www.readbyqxmd.com/read/28225063/targeted-inhibition-of-focal-adhesion-kinase-attenuates-cardiac-fibrosis-and-preserves-heart-function-in-adverse-cardiac-remodeling
#2
Jie Zhang, Guangpu Fan, Hui Zhao, Zhiwei Wang, Fei Li, Peide Zhang, Jing Zhang, Xu Wang, Wei Wang
Cardiac fibrosis in post-myocardial infarction (MI), seen in both infarcted and non-infarcted myocardium, is beneficial to the recovery of heart function. But progressively pathological fibrosis impairs ventricular function and leads to poor prognosis. FAK has recently received attention as a potential mediator of fibrosis, our previous study reported that pharmacological inhibition of FAK can attenuate cardiac fibrosis in post MI models. However, the long-term effects on cardiac function and adverse cardiac remodelling were not clearly investigated...
February 22, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28224334/the-trpm4-channel-is-functionally-important-for-the-beneficial-cardiac-remodeling-induced-by-endurance-training
#3
Mélanie Gueffier, Justin Zintz, Karen Lambert, Amanda Finan, Franck Aimond, Nourdine Chakouri, Christophe Hédon, Mathieu Granier, Pierre Launay, Jérôme Thireau, Sylvain Richard, Marie Demion
Cardiac hypertrophy (CH) is an adaptive process that exists in two distinct forms and allows the heart to adequately respond to an organism's needs. The first form of CH is physiological, adaptive and reversible. The second is pathological, irreversible and associated with fibrosis and cardiomyocyte death. CH involves multiple molecular mechanisms that are still not completely defined but it is now accepted that physiological CH is associated more with the PI3-K/Akt pathway while the main signaling cascade activated in pathological CH involves the Calcineurin-NFAT pathway...
February 21, 2017: Journal of Muscle Research and Cell Motility
https://www.readbyqxmd.com/read/28216385/the-role-of-mitochondria-in-cardiac-development-and-protection
#4
REVIEW
Jaakko L Pohjoismäki, Steffi Goffart
Mitochondria are essential for the development as well as maintenance of the myocardium, the most energy consuming tissue in the human body. Mitochondria are not only a source of ATP energy but also generators of reactive oxygen species (ROS), that cause oxidative damage, but also regulate physiological processes such as the switch from hyperplastic to hypertrophic growth after birth. As excess ROS production and oxidative damage are associated with cardiac pathology, it is not surprising that much of the research focused on the deleterious aspects of free radicals...
February 16, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28213819/conditional-knockout-of-activin-like-kinase-1-alk-1-leads-to-heart-failure-without-maladaptive-remodeling
#5
Kevin J Morine, Xiaoying Qiao, Vikram Paruchuri, Mark J Aronovitz, Emily E Mackey, Lyanne Buiten, Jonathan Levine, Keshan Ughreja, Prerna Nepali, Robert M Blanton, Richard H Karas, S Paul Oh, Navin K Kapur
Activin like kinase-1 (AlK-1) mediates signaling via the transforming growth factor beta (TGFβ) family of ligands. AlK-1 activity promotes endothelial proliferation and migration. Reduced AlK-1 activity is associated with arteriovenous malformations. No studies have examined the effect of global AlK-1 deletion on indices of cardiac remodeling. We hypothesized that reduced levels of AlK-1 promote maladaptive cardiac remodeling. To test this hypothesis, we employed AlK-1 conditional knockout mice (cKO) harboring the ROSA26-CreER knock-in allele, whereby a single dose of intraperitoneal tamoxifen triggered ubiquitous Cre recombinase-mediated excision of floxed AlK-1 alleles...
February 17, 2017: Heart and Vessels
https://www.readbyqxmd.com/read/28192468/matrix-metalloproteinases-are-required-for-membrane-motility-and-lumenogenesis-during-drosophila-heart-development
#6
Qanber S Raza, Jessica L Vanderploeg, J Roger Jacobs
Matrix Metalloproteinases (Mmps) degrade glycoproteins and proteoglycans of the extracellular matrix (ECM) or cell surface and are crucial for morphogenesis. Mmps and their inhibitors are expressed during early stages of cardiac development in vertebrates and expression is altered in multiple congenital cardiomyopathies such as cardia bifida. Drosophila genome encodes two copies of Mmps, Mmp1 and Mmp2 whereas in humans up to 25 Mmps have been identified with overlapping functions. We investigated the role of Mmps during embryonic heart development in Drosophila, a process which is morphogenetically similar to early heart tube formation in vertebrates...
2017: PloS One
https://www.readbyqxmd.com/read/28178567/defective-branched-chain-amino-acid-catabolism-disrupts-glucose-metabolism-and-sensitizes-the-heart-to-ischemia-reperfusion-injury
#7
Tao Li, Zhen Zhang, Stephen C Kolwicz, Lauren Abell, Nathan D Roe, Maengjo Kim, Bo Zhou, Yang Cao, Julia Ritterhoff, Haiwei Gu, Daniel Raftery, Haipeng Sun, Rong Tian
Elevated levels of branched-chain amino acids (BCAAs) have recently been implicated in the development of cardiovascular and metabolic diseases, but the molecular mechanisms are unknown. In a mouse model of impaired BCAA catabolism (knockout [KO]), we found that chronic accumulation of BCAAs suppressed glucose metabolism and sensitized the heart to ischemic injury. High levels of BCAAs selectively disrupted mitochondrial pyruvate utilization through inhibition of pyruvate dehydrogenase complex (PDH) activity...
February 7, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28159809/cardiac-med1-deletion-promotes-early-lethality-cardiac-remodeling-and-transcriptional-reprogramming
#8
Kathryn M Spitler, Jessica M Ponce, Gavin Y Oudit, Duane D Hall, Chad E Grueter
The Mediator complex, a multisubunit nuclear complex, plays an integral role in regulating gene expression by acting as a bridge between transcription factors and RNA polymerase II. Genetic deletion of mediator subunit 1 (Med1) results in embryonic lethality, due in large part to impaired cardiac development. We first established that Med1 is dynamically expressed in cardiac development and disease, with marked upregulation of Med1 in both human and murine failing hearts. To determine if Med1 deficiency protects against cardiac stress, we generated two cardiac-specific Med1 knockout mouse models in which Med1 is conditionally deleted (Med1cKO mice) or inducibly deleted in adult mice (Med1cKO-MCM mice)...
February 3, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28156163/post-infarct-sleep-disruption-and-its-relation-to-cardiac-remodeling-in-a-rat-model-of-myocardial-infarction
#9
Marjan Aghajani, Mahdieh Faghihi, Alireza Imani, Mohammad Reza Vaez Mahdavi, Abbas Shakoori, Tayebeh Rastegar, Hoda Parsa, Saman Mehrabi, Fatemeh Moradi, Ehsan Kazemi Moghaddam
Sleep disruption after myocardial infarction (MI) by affecting ubiquitin-proteasome system (UPS) is thought to contribute to myocardial remodeling and progressive worsening of cardiac function. The aim of current study was to test the hypothesis about the increased risk of developing heart failure due to experience of sleep restriction (SR) after MI. Male Wistar rats (n = 40) were randomly assigned to four experimental groups: (1) Sham, (2) MI, (3) MI and SR (MI + SR) (4) Sham and SR (Sham + SR). MI was induced by permanent ligation of left anterior descending coronary artery...
February 3, 2017: Chronobiology International
https://www.readbyqxmd.com/read/28155613/functional-upregulation-of-stim-1-orai-1-mediated-store-operated-ca2-contributing-to-the-hypertension-development-elicited-by-chronic-etoh-consumption
#10
Guilherme Henrique Souza Bomfim, Iago Méndez-López, Juan Alberto Arranz-Tagarro, Adriana Aparecida Ferraz Carbonel, Danilo Roman-Campos, Juan Fernando Padín, Antonio García García, Aron Jurkiewicz, Neide Hyppolito Jurkiewicz
Chronic ethanol (EtOH) consumption has been associated with deleterious effects on the cardiovascular system by abnormal calcium (Ca²⁺) handling. Store-operated Ca2+ entry (SOCE) is related to cardiovascular remodeling which leads to the hypertension development, and the coupling between STIM-1 (ER Ca2+ sensor) and Orai-1 (channel pore) is a key mechanism to control SOCE through of store-operated Ca2+ channels (SOCCs). However, the role of STIM-1/Orai-1-mediated SOCE and its cross-talk with EtOH-triggered vascular remodeling and hypertension remain poorly understood...
February 1, 2017: Current Vascular Pharmacology
https://www.readbyqxmd.com/read/28154134/cdon-deficiency-causes-cardiac-remodeling-through-hyperactivation-of-wnt-%C3%AE-catenin-signaling
#11
Myong-Ho Jeong, Hyun-Ji Kim, Jung-Hoon Pyun, Kyu-Sil Choi, Dong I Lee, Soroosh Solhjoo, Brian O'Rourke, Gordon F Tomaselli, Dong Seop Jeong, Hana Cho, Jong-Sun Kang
On pathological stress, Wnt signaling is reactivated and induces genes associated with cardiac remodeling and fibrosis. We have previously shown that a cell surface receptor Cdon (cell-adhesion associated, oncogene regulated) suppresses Wnt signaling to promote neuronal differentiation however its role in heart is unknown. Here, we demonstrate a critical role of Cdon in cardiac function and remodeling. Cdon is expressed and predominantly localized at intercalated disk in both mouse and human hearts. Cdon-deficient mice develop cardiac dysfunction including reduced ejection fraction and ECG abnormalities...
February 2, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28151473/knockout-of-eva1a-leads-to-rapid-development-of-heart-failure-by-impairing-autophagy
#12
Shu Zhang, Xin Lin, Ge Li, Xue Shen, Di Niu, Guang Lu, Xin Fu, Yingyu Chen, Ming Cui, Yun Bai
EVA1A (Eva-1 homologue A) is a novel lysosome and endoplasmic reticulum-associated protein that can regulate cell autophagy and apoptosis. Eva1a is expressed in the myocardium, but its function in myocytes has not yet been investigated. Therefore, we generated inducible, cardiomyocyte-specific Eva1a knockout mice with an aim to determine the role of Eva1a in cardiac remodelling in the adult heart. Data from experiments showed that loss of Eva1a in the adult heart increased cardiac fibrosis, promoted cardiac hypertrophy, and led to cardiomyopathy and death...
February 2, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28137415/analysis-of-mmp-7-and-timp-2-gene-polymorphisms-in-coronary-artery-disease-and-myocardial-infarction-a-turkish-case-control-study
#13
Ebru Alp, Akin Yilmaz, Murat Tulmac, Asiye Ugras Dikmen, Atiye Cengel, Ridvan Yalcin, Emine Sevda Menevse
Matrix metalloproteinase (MMP) and tissue inhibitors of metalloproteinase (TIMP) have a significant role in tissue remodeling related to cardiac function. In earlier studies, MMP-7 A-181G (rs11568818), C-153T (rs11568819), C-115T (rs17886546), and TIMP-2 G-418C (rs8179090) polymorphisms have been studied in various diseases. However, association between coronary artery disease (CAD) and these polymorphisms has been poorly studied. The goal of this study is to investigate the association of CAD and myocardial infarction (MI) with MMP-7 or TIMP-2 polymorphisms...
February 2017: Kaohsiung Journal of Medical Sciences
https://www.readbyqxmd.com/read/28132040/erectile-dysfunction-as-a-predictor-of-cardiovascular-disease
#14
Sh Janjgava, T Doliashvili
Endothelial dysfunction precedes the clinical stage of atherosclerotic disease and is recognized as an additional risk factor when detecting symptomatic patients. Endothelial function is largely mediated by nitric oxide, and this vasodilatory mechanism is also responsible for the venous and arterial dilatation required to obtain and maintain an erection. The physiological effects and clinical aspects of sexual function have been extensively studied and reported in patients who have angina or who have experienced a myocardial infarction and in those who have undergone coronary artery bypass graft surgery or heart transplant...
December 2016: Georgian Medical News
https://www.readbyqxmd.com/read/28131398/recombinant-%C3%AE-klotho-may-be-prophylactic-and-therapeutic-for-acute-to-chronic-kidney-disease-progression-and-uremic-cardiomyopathy
#15
Ming Chang Hu, Mingjun Shi, Nancy Gillings, Brianna Flores, Masaya Takahashi, Makoto Kuro-O, Orson W Moe
α-Klotho is highly expressed in the kidney, and its extracellular domain is cleaved and released into the circulation. Chronic kidney disease (CKD) is a state of α-Klotho deficiency, which exerts multiple negative systemic effects on numerous organs including the cardiovascular system. Since acute kidney injury (AKI) greatly escalates the risk of CKD development, we explored the effect of α-Klotho on prevention and treatment on post-AKI to CKD progression and cardiovascular disease. Therein, ischemia reperfusion injury-induced AKI was followed by early administration of recombinant α-Klotho or vehicle starting one day and continued for four days after kidney injury (CKD prevention protocol)...
January 25, 2017: Kidney International
https://www.readbyqxmd.com/read/28129334/a-novel-positron-emission-tomography-pet-approach-to-monitor-cardiac-metabolic-pathway-remodeling-in-response-to-sunitinib-malate
#16
Alice C O'Farrell, Rhys Evans, Johanna M U Silvola, Ian S Miller, Emer Conroy, Suzanne Hector, Maurice Cary, David W Murray, Monika A Jarzabek, Ashwini Maratha, Marina Alamanou, Girish Mallya Udupi, Liam Shiels, Celine Pallaud, Antti Saraste, Heidi Liljenbäck, Matti Jauhiainen, Vesa Oikonen, Axel Ducret, Paul Cutler, Fionnuala M McAuliffe, Jacques A Rousseau, Roger Lecomte, Suzanne Gascon, Zoltan Arany, Bonnie Ky, Thomas Force, Juhani Knuuti, William M Gallagher, Anne Roivainen, Annette T Byrne
Sunitinib is a tyrosine kinase inhibitor approved for the treatment of multiple solid tumors. However, cardiotoxicity is of increasing concern, with a need to develop rational mechanism driven approaches for the early detection of cardiac dysfunction. We sought to interrogate changes in cardiac energy substrate usage during sunitinib treatment, hypothesising that these changes could represent a strategy for the early detection of cardiotoxicity. Balb/CJ mice or Sprague-Dawley rats were treated orally for 4 weeks with 40 or 20 mg/kg/day sunitinib...
2017: PloS One
https://www.readbyqxmd.com/read/28123181/reverse-electrical-remodeling-following-pressure-unloading-in-a-rat-model-of-hypertension-induced-left-ventricular-myocardial-hypertrophy
#17
Mihály Ruppert, Sevil Korkmaz-Icöz, Shiliang Li, Béla Merkely, Matthias Karck, Tamás Radovits, Gábor Szabó
Pressure overload-induced left ventricular myocardial hypertrophy (LVH) is characterized by increased proarrhythmic vulnerability. In contrast, pressure unloading leads to reverse remodeling and decreases LVH-associated arrhythmogenicity. However, cellular changes that occur during reverse electrical remodeling have been studied less. Therefore, we aimed to provide an electrocardiographic characterization of a rat model of LVH that underwent pressure unloading and to simultaneously identify the underlying cellular and functional alterations...
January 26, 2017: Hypertension Research: Official Journal of the Japanese Society of Hypertension
https://www.readbyqxmd.com/read/28116799/in-vitro-models-of-the-cardiac-microenvironment-to-study-myocyte-and-non-myocyte-crosstalk-bioinspired-approaches-beyond-the-polystyrene-dish
#18
Celinda M Kofron, Ulrike Mende
The heart is a complex pluricellular organ comprised of cardiomyocytes and non-myocytes, including fibroblasts, endothelial cells, and immune cells. Myocytes are responsible for electrical conduction and contractile force generation, while the other cell types are responsible for matrix deposition, vascularization, and injury response. Myocytes and non-myocytes are known to communicate and exert mutual regulatory effects. In concert, they determine the structural, electrical, and mechanical characteristics in the healthy and remodeled myocardium...
January 23, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28116550/implantation-of-a-poly-l-lactide-gcsf-functionalized-scaffold-in-a-model-of-chronic-myocardial-infarction
#19
Cristiano Spadaccio, Francesco Nappi, Federico De Marco, Pietro Sedati, Chiara Taffon, Antonio Nenna, Anna Crescenzi, Massimo Chello, Marcella Trombetta, Ivancarmine Gambardella, Alberto Rainer
A previously developed poly-L-lactide scaffold releasing granulocyte colony-stimulating factor (PLLA/GCSF) was tested in a rabbit chronic model of myocardial infarction (MI) as a ventricular patch. Control groups were constituted by healthy, chronic MI and nonfunctionalized PLLA scaffold. PLLA-based electrospun scaffold efficiently integrated into a chronic infarcted myocardium. Functionalization of the biopolymer with GCSF led to increased fibroblast-like vimentin-positive cellular colonization and reduced inflammatory cell infiltration within the micrometric fiber mesh in comparison to nonfunctionalized scaffold; PLLA/GCSF polymer induced an angiogenetic process with a statistically significant increase in the number of neovessels compared to the nonfunctionalized scaffold; PLLA/GCSF implanted at the infarcted zone induced a reorganization of the ECM architecture leading to connective tissue deposition and scar remodeling...
January 23, 2017: Journal of Cardiovascular Translational Research
https://www.readbyqxmd.com/read/28115807/functional-remodeling-of-both-atria-is-associated-with-occurrence-of-stroke-in-patients-with-paroxysmal-and-persistent-atrial-fibrillation
#20
Hsuan-Ming Tsao, Wei-Chih Hu, Ping-Huang Tsai, Chao-Lin Lee, Hsueh-Han Wang, Shih-Lin Chang, Tze-Fan Chao, Shih-Ann Chen
BACKGROUND: It is critical to recognize high risk patients who are prone to develop stroke in the management of atrial fibrillation (AF). The purpose of this study was to identify the determinants of AF related stroke by assessing the anatomical and functional remodeling of cardiac chambers. METHODS: We compared the cardiac structure and function of 28 consecutive patients with paroxysmal and persistent AF-related stroke with 69 patients with AF and 21 controls without stroke using contrast-enhanced 64-slice multi-detector computed tomography during sinus rhythm...
January 2017: Acta Cardiologica Sinica
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