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Journal of Molecular and Cellular Cardiology

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https://www.readbyqxmd.com/read/30118791/anti-androgenic-therapy-with-finasteride-improves-cardiac-function-attenuates-remodeling-and-reverts-pathologic-gene-expression-after-myocardial-infarction-in-mice
#1
Natali Froese, Honghui Wang, Carolin Zwadlo, Yong Wang, Andrea Grund, Anna Gigina, Melanie Hofmann, Katja Kilian, Gesine Scharf, Mortimer Korf-Klingebiel, Anna Melchert, Maria Elena Ricci Signorini, Caroline Halloin, Robert Zweigerdt, Ulrich Martin, Ina Gruh, Kai C Wollert, Robert Geffers, Johann Bauersachs, Joerg Heineke
Maladaptive cardiac remodeling after myocardial infarction (MI) is increasingly contributing to the prevalence of chronic heart failure. Women show less severe remodeling, a reduced mortality and a better systolic function after MI compared to men. Although sex hormones are being made responsible for these differences, it remains currently unknown how this could be translated into therapeutic strategies. Because we had recently demonstrated that inhibition of the conversion of testosterone to its highly active metabolite dihydrotestosterone (DHT) by finasteride effectively reduces cardiac hypertrophy and improves heart function during pressure overload, we asked here whether this strategy could be applied to post-MI remodeling...
August 14, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30118790/ischemic-preconditioning-protects-against-cardiac-ischemia-reperfusion-injury-without-affecting-succinate-accumulation-or-oxidation
#2
Victoria R Pell, Ana-Mishel Spiroski, John Mulvey, Nils Burger, Ana S H Costa, Angela Logan, Anja V Gruszczyk, Tiziana Rosa, Andrew M James, Christian Frezza, Michael P Murphy, Thomas Krieg
Ischemia-reperfusion (IR) injury occurs when blood supply to an organ is disrupted and then restored, and underlies many disorders, notably myocardial infarction and stroke. While reperfusion of ischemic tissue is essential for survival, it also initiates cell death through generation of mitochondrial reactive oxygen species (ROS). Recent work has revealed a novel pathway underlying ROS production at reperfusion in vivo in which the accumulation of succinate during ischemia and its subsequent rapid oxidation at reperfusion drives ROS production at complex I by reverse electron transport (RET)...
August 14, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30118789/the-emerging-landscape-of-circular-rna-in-cardiovascular-diseases
#3
REVIEW
Meng-Yuan Zhou, Jin-Ming Yang, Xing-Dong Xiong
Circular RNAs (circRNAs), a large novel type of endogenous transcripts, have become a new research hotspot in the field of RNA biology. CircRNAs are mainly generated from exons or introns via multiple mechanisms, and the majority of circRNAs are stable and conserved across different species. Recent studies have revealed that circRNAs can function as miRNA sponges, binding partners of proteins, regulators of transcription, or can even be translated into proteins. Growing evidence has demonstrated that circRNAs play important roles in a wide variety of biological processes such as cell proliferation, apoptosis and senescence, and may serve as potential diagnostic biomarkers or therapeutic targets for various cardiovascular diseases...
August 14, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30114394/activation-of-tp-receptors-induces-high-release-of-pgi-2-in-coronary-arteries-of-renal-hypertensive-rats
#4
T D Paula, B R Silva, M D Grando, H C D Souza, L M Bendhack
AIM: To investigate the molecular mechanisms and cellular signaling pathways involved in the activation of TP receptors and the consequent induction of contractile responses in coronary arteries of renal hypertensive (2K-1C) rats. METHODS AND RESULTS: The coronary perfusion pressure (CPP) was lower in 2K-1C rats during increased coronary flow as measured by the Langendorff technique. The coronary contraction and relaxation were evaluated by vascular reactivity studies, and the molecular mechanisms were investigated on the basis of the protein expression of TP receptors, Cav-1, eNOS, COX-1, and COX-2, as measured by Western blot...
August 13, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30102883/cardiac-specific-knockout-of-lmod2-results-in-a-severe-reduction-in-myofilament-force-production-and-rapid-cardiac-failure
#5
Christopher T Pappas, Gerrie P Farman, Rachel M Mayfield, John P Konhilas, Carol C Gregorio
Leiomodin-2 (Lmod2) is a striated muscle-specific actin binding protein that is implicated in assembly of thin filaments. The necessity of Lmod2 in the adult mouse and role it plays in the mechanics of contraction are unknown. To answer these questions, we generated cardiac-specific conditional Lmod2 knockout mice (cKO). These mice die within a week of induction of the knockout with severe left ventricular systolic dysfunction and little change in cardiac morphology. Cardiac trabeculae isolated from cKO mice have a significant decrease in maximum force production and a blunting of myofilament length-dependent activation...
August 10, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30098988/protease-activated-receptor-1-activation-enhances-doxorubicin-induced-cardiotoxicity
#6
Silvio Antoniak, Kohei Tatsumi, Clare M Schmedes, Steven P Grover, Rafal Pawlinski, Nigel Mackman
OBJECTIVE: The anti-cancer anthracycline drug Doxorubicin (Dox) causes cardiotoxicity. We investigated the role of protease-activated receptor 1 (PAR-1) in Dox-induced cardiotoxicity. METHODS AND RESULTS: In vitro experiments revealed that PAR-1 enhanced Dox-induced mitochondrial dysfunction, reactive oxygen species and cell death of cardiac myocytes and cardiac fibroblasts. The contribution of PAR-1 to Dox-induced cardiotoxicity was investigated by subjecting PAR-1-/- mice and PAR-1+/+ mice to acute and chronic exposure to Dox...
August 9, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30098987/inhibition-of-erk-drp1-signaling-and-mitochondria-fragmentation-alleviates-igf-iir-induced-mitochondria-dysfunction-during-heart-failure
#7
Chih-Yang Huang, Chao-Hung Lai, Chia-Hua Kuo, Shu-Fen Chiang, Pei-Ying Pai, Jing-Ying Lin, Chih-Fen Chang, Vijaya Padma Viswanadha, Wei-Wen Kuo, Chih-Yang Huang
Mitochondrial dysfunction is a major contributor to myocyte loss and the development of heart failure. Myocytes have quality control mechanisms to retain functional mitochondria by removing damaged mitochondria via specialized autophagy, i.e., mitophagy. The underlying mechanisms of fission affect the survival of cardiomyocytes, and left ventricular function in the heart is poorly understood. Here, we demonstrated the direct effect and potential mechanisms of mitochondrial functional defects associated with abnormal mitochondrial dynamics in heart failure...
August 9, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30098321/the-salient-role-of-micrornas-in-atherogenesis
#8
REVIEW
Callum J Donaldson, Ka Hou Lao, Lingfang Zeng
Atherosclerosis, a chronic inflammatory condition that is characterized by the accumulation of lipid-loaded macrophages, occurs preferentially at the arterial branching points where disturbed flow is prominent. The pathogenesis of atherosclerotic lesion formation is a multistage process involving multiple cell types, inflammatory mediators and hemodynamic forces in the vessel wall in response to atherogenic stimuli. Researches from the past decade have uncovered the critical roles of microRNAs (miRNAs) in regulating multiple pathophysiological effects and signaling pathways in endothelial cells (ECs), vascular smooth muscle cells (VSMCs), macrophages and lipid homeostasis, which are key in atherosclerotic lesion formation...
August 8, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30096409/interleukin-17-enhances-cardiac-ventricular-remodeling-via-activating-mapk-pathway-in-ischemic-heart-failure
#9
Shih-Lin Chang, Ya-Wen Hsiao, Yung-Nan Tsai, Shien-Fong Lin, Shuen-Hsin Liu, Yenn-Jiang Lin, Li-Wei Lo, Fa-Po Chung, Tze-Fan Chao, Yu-Feng Hu, Ta-Chuan Tuan, Jo-Nan Liao, Yu-Cheng Hsieh, Tsu-Juey Wu, Satoshi Higa, Shih-Ann Chen
BACKGROUND: We aimed to investigate the impact of interleukin (IL)-17 on ventricular remodeling and the genesis of ventricular arrhythmia (VA) in an ischemic heart failure (HF) model. The expression of the proinflammatory cytokine IL-17 is upregulated during myocardial ischemia and plays a fundamental role in postinfarct inflammation. However, the influence of IL-17 on the genesis of VA has not yet been studied. METHODS AND RESULTS: The level of inflammation and Th17 cell (CD4+ IL-17+ ) expression in the rabbit model of ischemic HF were studied by flow cytometry, quantitative polymerase chain reaction (qPCR), and enzyme-linked immunosorbent assay (ELISA)...
August 7, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30096408/sympathoadrenergic-suppression-improves-heart-function-by-upregulating-the-ratio-of-srage-rage-in-hypertension-with-metabolic-syndrome
#10
Simina-Ramona Selejan, Dominik Linz, Anna-Maria Tatu, Mathias Hohl, Thimoteus Speer, Sebastian Ewen, Felix Mahfoud, Ingrid Kindermann, Olesja Zamyatkin, Andrey Kazakov, Ulrich Laufs, Michael Böhm
Receptors-for-Advanced-Glycation-End-products (RAGE) activate pro-inflammatory programs mediated by carboxymethyllysine (CML) and high-mobility-group-box1 protein (HMGB1). The soluble isoform sRAGE neutralizes RAGE-ligands preventing cardiovascular complications in conditions associated with increased sympathetic activation like hypertension and diabetes. The effects of sympathetic modulation on RAGE/sRAGE-balance and end-organ damage in metabolic syndrome on top of hypertension remains unknown. We hypothesized that increased sympathoadrenergic activity might lead to an unfavourable RAGE/sRAGE regulation...
August 7, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30096407/the-nuclear-receptor-nor-1-modulates-redox-homeostasis-in-human-vascular-smooth-muscle-cells
#11
Judith Alonso, Laia Cañes, Ana B García-Redondo, Pablo García de Frutos, Cristina Rodríguez, José Martínez-González
No abstract text is available yet for this article.
August 7, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30092227/lysine-glycation-of-apolipoprotein-a-i-impairs-its-anti-inflammatory-function-in-type-2-diabetes-mellitus
#12
Donghui Liu, Liang Ji, Mingming Zhao, Yang Wang, Yansong Guo, Ling Li, Dongmei Zhang, Liang Xu, Bing Pan, Jinzi Su, Song Xiang, Subramaniam Pennathur, Jingxuan Li, Jianing Gao, Pingsheng Liu, Belinda Willard, Lemin Zheng
Apolipoprotein A-I (apoA-I), the major protein compontent of high-density lipoprotein (HDL), exerts many anti-atherogenic functions. This study aimed to reveal whether nonenzymatic glycation of specific sites of apoA-I impaired its anti-inflammatory effects in type 2 diabetes mellitus (T2DM). LC-MS/MS was used to analyze the specific sites and the extent of apoA-I glycation either modified by glucose in vitro or isolated from T2DM patients. Cytokine release in THP-1 monocyte-derived macrophages was tested by ELISA...
August 6, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30063898/hdac11-regulates-interleukin-13-expression-in-cd4-t-cells-in-the-heart
#13
Li Yuan, Xiao Chen, Liang Cheng, Man Rao, Kai Chen, Ningning Zhang, Jian Meng, Mengmeng Li, Li-Tao Yang, Ping-Chang Yang, Xin Wang, Jiangping Song
BACKGROUND AND AIMS: Immune deregulation is a causative factor in pathogenesis of myocarditis. Histone deacetylases (HDAC) involve multiple biochemical activities in the cell. This study aims to elucidate the role of HDAC11 in the regulation of interleukin (IL)-13-expression in CD4+ T cells of heart tissue in patients with myocarditis (MCD). METHODS: After heart transplantation, surgically removed hearts were collected from patients with advanced heart failure and MCD or dilated cardiomyopathy (DCM)...
July 29, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30009777/restoration-of-cardiac-function-after-anaemia-induced-heart-failure-in-zebrafish
#14
Isabelle Ernens, Andrew I Lumley, Yvan Devaux
AIMS: New therapeutic approaches are needed to fight against the growing epidemic of heart failure. Unlike mammals, zebrafish possess the incredible ability to regenerate cardiac tissue after acute trauma such as apical resection. Yet, the ability of zebrafish to recover after a chronic stress leading to heart failure has not been reported. The aim of this study was to test whether zebrafish can recover a normal cardiac function after anaemia-induced heart failure. METHODS AND RESULTS: Eight- to ten-month-old zebrafish were treated with phenylhydrazine hydrochloride, an anaemia inducer, to generate heart failure...
July 26, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30053527/microrna-101a-suppresses-fibrotic-programming-in-isolated-cardiac-fibroblasts-and-in-vivo-fibrosis-following-trans-aortic-constriction
#15
Yue Zhou, Thiam Chien Shiok, Arthur Mark Richards, Peipei Wang
AIMS: MiR-101a is reported to reduce post-infarction myocardial fibrosis through targeting c-FOS and TGFbr1. However the actions of miR-101a within the TGF-β signaling pathway are largely unknown. We demonstrate the mechanisms underlying mutual inhibition between miR-101a and TGF-β signaling and explore the therapeutic potential of miR-101a in suppressing pressure overload-induced cardiac fibrosis. METHODS AND RESULTS: The effects of miR-101a on fibroblast proliferation, myofibroblast transdifferentiation, collagen synthesis, apoptosis, and autophagy were assessed in isolated rat cardiac fibroblasts (cFB)...
July 24, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30053526/genetic-lineage-tracing-analysis-of-c-kit-stem-progenitor-cells-revealed-a-contribution-to-vascular-injury-induced-neointimal-lesions
#16
Qishan Chen, Mei Yang, Hong Wu, Jiaojiao Zhou, Weina Wang, Hongkun Zhang, Lin Zhao, Jianhua Zhu, Bin Zhou, Qingbo Xu, Li Zhang
AIMS: Accumulating evidence indicates the presence of vascular stem/progenitor cells that may play a role in endothelial repair and lesion formation in the injured artery, in which c-kit+ stem/progenitor cells have been reported to differentiate into endothelial and smooth muscle cells in vitro and in ischemic tissue. In this study, we investigated whether and how endogenous c-kit+ stem/progenitor cells contribute to vascular injury and neointima formation in vivo. METHODS AND RESULTS: We created Kit-CreERxRosa26-RFP mice and performed genetic lineage tracing analysis of c-kit+ stem/progenitor cells in injury-induced neointima formation in vivo...
July 24, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30053525/irisin-alleviates-pressure-overload-induced-cardiac-hypertrophy-by-inducing-protective-autophagy-via-mtor-independent-activation-of-the-ampk-ulk1-pathway
#17
Ru-Li Li, Si-Si Wu, Yao Wu, Xiao-Xiao Wang, Hong-Ying Chen, Juan-Juan Xin, He Li, Jie Lan, Kun-Yue Xue, Xue Li, Cai-Li Zhuo, Yu-Yan Cai, Jin-Han He, Heng-Yu Zhang, Chao-Shu Tang, Wang Wang, Wei Jiang
In hypertrophic hearts, autophagic flux insufficiency is recognized as a key pathology leading to maladaptive cardiac remodeling and heart failure. This study aimed to illuminate the cardioprotective role and mechanisms of a new myokine and adipokine, irisin, in cardiac hypertrophy and remodeling. Adult male wild-type, mouse-FNDC5 (irisin-precursor)-knockout and FNDC5 transgenic mice received 4 weeks of transverse aortic constriction (TAC) alone or combined with intraperitoneal injection of chloroquine diphosphate (CQ)...
July 24, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30053524/deletion-of-calponin-2-attenuates-the-development-of-calcific-aortic-valve-disease-in-apoe-mice
#18
Olesya Plazyo, Rong Liu, M Moazzem Hossain, J-P Jin
Calcific aortic valve disease (CAVD) is a leading cause of cardiovascular mortality and lacks non-surgical treatment. The pathogenesis of CAVD involves perturbation of valvular cells by mechanical stimuli, including shear stress, pressure load and leaflet stretch, of which the molecular mechanism requires further elucidation. We recently demonstrated that knockout (KO) of Cnn2 gene that encodes calponin isoform 2, a mechanoregulated cytoskeleton protein, attenuates atherosclerosis in ApoE KO mice. Here we report that Cnn2 KO also decreased calcification of the aortic valve in ApoE KO mice, an established model of CAVD...
July 24, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30048712/mutant-muscle-lim-protein-c58g-causes-cardiomyopathy-through-protein-depletion
#19
Mehroz Ehsan, Matthew Kelly, Charlotte Hooper, Arash Yavari, Julia Beglov, Mohamed Bellahcene, Kirandeep Ghataorhe, Giulia Poloni, Anuj Goel, Theodosios Kyriakou, Karin Fleischanderl, Elisabeth Ehler, Eugene Makeyev, Stephan Lange, Houman Ashrafian, Charles Redwood, Benjamin Davies, Hugh Watkins, Katja Gehmlich
Cysteine and glycine rich protein 3 (CSRP3) encodes Muscle LIM Protein (MLP), a well-established disease gene for Hypertrophic Cardiomyopathy (HCM). MLP, in contrast to the proteins encoded by the other recognised HCM disease genes, is non-sarcomeric, and has important signalling functions in cardiomyocytes. To gain insight into the disease mechanisms involved, we generated a knock-in mouse (KI) model, carrying the well documented HCM-causing CSRP3 mutation C58G. In vivo phenotyping of homozygous KI/KI mice revealed a robust cardiomyopathy phenotype with diastolic and systolic left ventricular dysfunction, which was supported by increased heart weight measurements...
July 23, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30048711/temperature-sensitive-sarcomeric-protein-post-translational-modifications-revealed-by-top-down-proteomics
#20
Wenxuan Cai, Zachary L Hite, Beini Lyu, Zhijie Wu, Ziqing Lin, Zachery R Gregorich, Andrew E Messer, Sean J McIlwain, Steve B Marston, Takushi Kohmoto, Ying Ge
Despite advancements in symptom management for heart failure (HF), this devastating clinical syndrome remains the leading cause of death in the developed world. Studies using animal models have greatly advanced our understanding of the molecular mechanisms underlying HF; however, differences in cardiac physiology and the manifestation of HF between animals, particularly rodents, and humans necessitates the direct interrogation of human heart tissue samples. Nevertheless, an ever-present concern when examining human heart tissue samples is the potential for artefactual changes related to temperature changes during tissue shipment or sample processing...
July 23, 2018: Journal of Molecular and Cellular Cardiology
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