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Cardiac fibrosis

Andrea I Guaricci, Delia De Santis, Mark G Rabbat, Gianluca Pontone
: Implantable cardioverter defibrillators (ICDs) have proven to be the most effective preventive therapy of sudden cardiac death (SCD). Based on current guidelines, the indication for prophylactic ICD therapy is primarily based on a left ventricular ejection fraction (LVEF) less than 35%. However, patients with low LVEF may never have an arrhythmic event while patients with normal to moderately reduced LVEF, who are traditionally felt to be at lower risk, can experience SCD. Therefore, LVEF alone is not an ideal risk stratification parameter to determine ICD therapy...
March 19, 2018: Journal of Cardiovascular Medicine
Vikram Subramanian, Sabine Borchard, Omid Azimzadeh, Wolfgang Sievert, Juliane Merl-Pham, Mariateresa Mancuso, Emanuela Pasquali, Gabriele Multhoff, Bastian Popper, Hans Zischka, Michael J Atkinson, Soile Tapio
High-dose ionizing radiation is known to induce adverse effects such as inflammation and fibrosis in the heart. Transcriptional regulators PPARα and TGFβ are known to be involved in this radiation response. PPARα, an anti-inflammatory transcription factor controlling cardiac energy metabolism, is inactivated by irradiation. The pro-inflammatory and pro-fibrotic TGFβ is activated by irradiation via SMAD-dependent and SMAD-independent pathways. The goal of this study was to investigate how altering the level of PPARα influences the radiation response of these signaling pathways...
March 21, 2018: Journal of Proteome Research
Jianjian Shi, Michelle Surma, Lei Wei
Doxorubicin is among the essential medicines with a wide antitumor spectrum, but its clinical application is limited by its cardiotoxicity. We recently discovered that ROCK1 is a key molecule in mediating cardiac remodeling in response to various stresses. To determine the roles of ROCK1 in doxorubicin cardiotoxicity, we gave three doses of doxorubicin injections to wild type (WT) and ROCK1-/- mice with one week intervals between treatments, the cumulative dose being 24 mg/kg. ROCK1-/- mice exhibited preserved cardiac function, reduced apoptosis, autophagy and fibrosis compared to the WT mice...
February 27, 2018: Oncotarget
Yang Dong, Dan Yang, Yuchi Han, Wei Cheng, Jiayu Sun, Ke Wan, Hong Liu, Andreas Greiser, Xiaoyue Zhou, Yucheng Chen
Background: Diffuse myocardial fibrosis is a common pathological process in many cardiovascular diseases. In order to determine disease, we must have standard normal imaging values. We investigated myocardial interstitial fibrosis of the left ventricle (LV) in a healthy population of Chinese adults and explored the impact of gender, age, and other physiological factors using a T1 mapping technique of cardiac magnetic resonance imaging (CMR). Materials and Methods: We recruited 69 healthy adult Chinese subjects (35 males; age 18-76)...
2018: Frontiers in Physiology
Adam Vandergriff, Ke Huang, Deliang Shen, Shiqi Hu, Michael Taylor Hensley, Thomas G Caranasos, Li Qian, Ke Cheng
Rationale: Cardiac stem cell-derived exosomes have been demonstrated to promote cardiac regeneration following myocardial infarction in preclinical studies. Recent studies have used intramyocardial injection in order to concentrate exosomes in the infarct. Though effective in a research setting, this method is not clinically appealing due to its invasive nature. We propose the use of a targeting peptide, cardiac homing peptide (CHP), to target intravenously-infused exosomes to the infarcted heart. Methods: Exosomes were conjugated with CHP through a DOPE-NHS linker...
2018: Theranostics
Akihiko Kimura, Yuko Ishida, Machi Furuta, Mizuho Nosaka, Yumi Kuninaka, Akira Taruya, Naofumi Mukaida, Toshikazu Kondo
BACKGROUND: A clear understanding of the molecular mechanisms underlying hemodynamic stress-initiated cardiac hypertrophy is important for preventing heart failure. Interferon-γ (IFN-γ) has been suggested to play crucial roles in various diseases other than immunological disorders by modulating the expression of myriad genes. However, the involvement of IFN-γ in the pathogenesis of cardiac hypertrophy still remains unclear. METHODS AND RESULTS: In order to elucidate the roles of IFN-γ in pressure overload-induced cardiac pathology, we subjected Balb/c wild-type (WT) or IFN-γ-deficient ( Ifng -/- ) mice to transverse aortic constriction (TAC)...
March 19, 2018: Journal of the American Heart Association
Shuyi Wang, Jun Ren
Alcoholism is accompanied with a high incidence of cardiac morbidity and mortality due to the development of alcoholic cardiomyopathy, manifested as dilation of one or both ventricles, reduced ventricular wall thickness, myofibrillary disarray, interstitial fibrosis, hypertrophy and contractile dysfunction. Several theories have been postulated for the etiology of alcoholic cardiomyopathy including ethanol/acetaldehyde toxicity, mitochondrial production of reactive oxygen species, oxidative injury, apoptosis, impaired myofilament Ca2+ sensitivity and protein synthesis, altered fatty acid extraction and deposition, as well as accelerated protein catabolism...
March 16, 2018: Biochimica et Biophysica Acta
Ming Hu, Zhenhui Zhang, Bin Liu, Shuangwei Zhang, Renjie Chai, Xiaohua Chen, Tianyu Kong, Fangcheng Zhang, Jingzhi Zhang, Shiming Liu, Ningning Liu
BACKGROUND/AIMS: Cardiac hypertrophy is a major outcome and compensatory response of the cardiovascular system to hemodynamic and additional stress responses that ultimately lead to heart failure. Auranofin (Aur) has been used for treating rheumatic arthritis for several decades. Aur is a 19S proteasome-associated deubiquitinase inhibitor, and inhibition of the proteasome is speculated to reverse cardiac hypertrophy. However, the role of the deubiquitinases, especially 19S proteasome-associated deubiquitinases, in the regulation of cardiac remodeling remains poorly understood...
March 15, 2018: Cellular Physiology and Biochemistry
Yogi Umbarawan, Mas Rizky A A Syamsunarno, Norimichi Koitabashi, Aiko Yamaguchi, Hirofumi Hanaoka, Takako Hishiki, Yoshiko Nagahata-Naito, Hideru Obinata, Motoaki Sano, Hiroaki Sunaga, Hiroki Matsui, Yoshito Tsushima, Makoto Suematsu, Masahiko Kurabayashi, Tatsuya Iso
Aims: The metabolism of the failing heart is characterized by an increase in glucose uptake with reduced fatty acid (FA) oxidation. We previously found that the genetic deletion of fatty acid binding protein-4 and -5 (DKO) induces an increased myocardial reliance on glucose with decreased FA uptake in mice. However, whether this fuel switch confers functional benefit during the hypertrophic response remains open to debate. To address this question, we investigated the contractile function and metabolic profile of DKO hearts subjected to pressure overload...
March 15, 2018: Cardiovascular Research
Ayako Uchinaka, Maho Yoshida, Kiyoka Tanaka, Yoshinosuke Hamada, Seiji Mori, Yoshitaka Maeno, Shigeru Miyagawa, Yoshiki Sawa, Kohzo Nagata, Hirofumi Yamamoto, Naomasa Kawaguchi
OBJECTIVE: Left ventricular (LV) remodeling alters the contractile and relaxation properties and induces myocardial stiffness. As LV remodeling progresses, the amount of collagen type III (Col3) is gradually decreased, being replaced by collagen type I (Col1). We evaluated whether Col3 overexpression improved cardiac function and remodeling in a rat with ischemic cardiomyopathy (ICM). We also investigated the functional motif and mechanism of thrombin-cleaved N-terminal osteopontin (N-OPN) on cardiac remodeling...
February 21, 2018: Journal of Thoracic and Cardiovascular Surgery
Chengliang Zhang, Yanfeng Zhang, Hong Zhu, Jiajia Hu, Zhongshang Xie
Cardiac fibrosis is associated with diverse heart diseases. In response to different pathological irritants, cardiac fibroblasts may be induced to proliferate and differentiate into cardiac myofibroblasts, thus contributing to cardiac fibrosis. TGF-β signaling is implicated in the development of heart failure through the induction of cardiac fibrosis. C-Ski, an inhibitory regulator of TGF-β signaling, has been reported to suppress TGF-β1-induced human cardiac fibroblasts' proliferation and ECM protein increase; however, the underlying molecular mechanism needs further investigation...
March 15, 2018: Cellular Signalling
Alessandro Zorzi, Angela Susana, Manuel De Lazzari, Federico Migliore, Giovanni Vescovo, Daniele Scarpa, Anna Baritussio, Giuseppe Tarantini, Luisa Cacciavillani, Benedetta Giorgi, Cristina Basso, Sabino Iliceto, Chiara Bucciarelli Ducci, Domenico Corrado, Martina Perazzolo Marra
BACKGROUND: In patients who survived out-of-hospital cardiac arrest (OHCA) it is crucial to establish the underlying cause and its potential reversibility. OBJECTIVE: We assessed the incremental diagnostic and prognostic role of early cardiac magnetic resonance (CMR) in survivors of OHCA. METHODS: Among 139 consecutive OHCA patients, we enrolled 44 (median age 43 years; 84% males) patients who underwent coronary angiography and CMR ≤7 days after admission...
March 14, 2018: Heart Rhythm: the Official Journal of the Heart Rhythm Society
Olivier Villemain, Mafalda Correia, Elie Mousseaux, Jérome Baranger, Samuel Zarka, Ilya Podetti, Gilles Soulat, Thibaud Damy, Albert Hagège, Mickael Tanter, Mathieu Pernot, Emmanuel Messas
OBJECTIVES: The goal of our study was to investigate the potential of myocardial shear wave imaging (SWI) to quantify the diastolic myocardial stiffness (MS) (kPa) noninvasively in adult healthy volunteers (HVs) and its physiological variation with age, and in hypertrophic cardiomyopathy (HCM) populations with heart failure and preserved ejection function (HFpEF). BACKGROUND: MS is an important prognostic and diagnostic parameter of the diastolic function. MS is affected by physiological changes but also by pathological alterations of extracellular and cellular tissues...
March 9, 2018: JACC. Cardiovascular Imaging
Muhammad Naveed, Lei Han, Ghulam Jilany Khan, Sufia Yasmeen, Reyaj Mikrani, Muhammad Abbas, Li Cunyu, Zhou Xiaohui
Congestive heart failure (CHF) is a complicated pathophysiological syndrome, leading cause of hospitalization as well as mortalities in developed countries wherein an irregular function of the heart leads to the insufficient blood supply to the body organs. It is an accumulative slackening of various complications including myocardial infarction (MI), coronary heart disease (CAD), hypertension, valvular heart disease (VHD) and cardiomyopathy; its hallmarks include hypertrophy, increased interstitial fibrosis and loss of myocytes...
March 14, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
Ana Isabel Padrão, Rita Nogueira-Ferreira, Rui Vitorino, Dulce Carvalho, Catarina Correia, Maria João Neuparth, Maria João Pires, Ana Isabel Faustino-Rocha, Lúcio Lara Santos, Paula Alexandra Oliveira, José Alberto Duarte, Daniel Moreira-Gonçalves, Rita Ferreira
Limiting cancer-induced cardiac damage has become an increasingly important issue to improve survival rates and quality of life. Exercise training has been shown to reduce cardiovascular complications in several diseases; however, its therapeutic role against cardiovascular consequences of cancer is in its infancy. In order to add new insights on the potential therapeutic effect of exercise training on cancer-related cardiac dysfunction, we used an animal model of urothelial carcinoma submitted to 13 weeks of treadmill exercise after 20 weeks of exposure to the carcinogenic N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN)...
March 13, 2018: Archives of Biochemistry and Biophysics
Olga Gruzdeva, Evgenya Uchasova, Yulia Dyleva, Daria Borodkina, Olga Akbasheva, Ekaterina Belik, Viktoria Karetnikova, Natalia Brel, Alexander Kokov, Vasiliy Kashtalap, Olga Barbarash
BACKGROUND: Determination of the impact of visceral obesity and epicardial adipose tissue thickness on stimulating growth factor levels during hospitalization for myocardial infarction is of potential importance for predicting outcomes and assessing the development of cardiofibrotic changes associated with maladaptive myocardial remodeling. In this study, we aimed to investigate the relationships between epicardial adipose tissue thickness, adipokine profiles, and the stimulating growth factor 2/interleukin-33 signaling system during hospitalization for myocardial infarction, and with the cardiac fibrosis extent 1-year post-MI in patients with visceral obesity...
March 16, 2018: Cardiovascular Diabetology
Taishi Nakamura, Guangshuo Zhu, Mark J Ranek, Kristen Kokkonen-Simon, Manling Zhang, Grace E Kim, Kenichi Tsujita, David A Kass
BACKGROUND: Stimulation of sGC (soluble guanylate cyclase) or inhibition of PDE5 (phosphodiesterase type 5) activates PKG (protein kinase G)-1α to counteract cardiac hypertrophy and failure. PKG1α acts within localized intracellular domains; however, its oxidation at cysteine 42, linking homomonomers, alters this localization, impairing suppression of pathological cardiac stress. Because PDE5 and sGC reside in separate microdomains, we speculated that PKG1α oxidation might also differentially influence the effects from their pharmacological modulation...
March 2018: Circulation. Heart Failure
Rasa Tamosiuniene, Olga Manouvakhova, Paul Mesange, Toshie Saito, Jin Qian, Mrinmoy Sanyal, Yu-Chun Lin, Linh P Nguyen, Amir Luria, Allen B Tu, Joshua M Sante, Marlene Rabinovitch, Desmond J Fitzgerald, Brian B Graham, Aida Habtezion, Norbert F Voelkel, Laure Aurelian, Mark R Nicolls
<u>Rationale:</u> Pulmonary arterial hypertension (PH) is a life-threatening condition associated with immune dysregulation and abnormal regulatory T cell (Treg) activity, but it is currently unknown whether and how abnormal Treg function differentially affects males and females. <u>Objective:</u> To evaluate whether and how Treg-deficiency differentially affects male and female rats in experimental PH. <u>Methods and Results:</u> Male and female athymic rnu/rnu rats, lacking Tregs, were treated with the vascular endothelial growth factor receptor-2 (VEGFR2) inhibitor SU5416 or chronic hypoxia and evaluated for PH; some animals underwent Treg immune reconstitution (IR) before SU5416 administration...
March 15, 2018: Circulation Research
Jaime Ibarrola, Rafael Sádaba, Amaia Garcia-Peña, Vanessa Arrieta, Ernesto Martinez-Martinez, Virginia Alvarez, Amaya Fernández-Celis, Alicia Gainza, Enrique Santamaría, Joaquin Fernández-Irigoyen, Victoria Cachofeiro, Renaud Fay, Patrick Rossignol, Natalia López-Andrés
AIMS: Galectin-3 (Gal-3), a β-galactoside-binding lectin involved in cardiac inflammation and fibrosis, could regulate oxidative stress, although the mechanisms have not been elucidated. We herein investigated the changes in oxidative stress-related mediators induced by Gal-3 in human cardiac fibroblasts and in pathological animal and human models of cardiac diseases. RESULTS: Using quantitative proteomics and immunodetection approaches, we have identified that Gal-3 down-regulated fumarate hydratase (FH) in human cardiac fibroblasts...
May 1, 2018: International Journal of Cardiology
Andrew R Kompa, Jiayu Lu, Thomas J Weller, Darren J Kelly, Henry Krum, Thomas G von Lueder, Bing H Wang
BACKGROUND: Angiotensin receptor neprilysin inhibitor (ARNi) enhances beneficial natriuretic peptides by inhibiting their breakdown through neprilysin. Although the first-in-class ARNi sacubitril/valsartan (LCZ696) reduced mortality and morbidity in heart failure (HF) with reduced ejection fraction (EF) compared to angiotensin converting enzyme inhibitor (ACEi), mechanistic data on ARNi are scarce. ARNi may be superior to ACEi in attenuating adverse cardiac remodeling and dysfunction post-myocardial infarction (MI)...
May 1, 2018: International Journal of Cardiology
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