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Cardiac development, cardiac remodelling, cardiac function

Wilfried Dinh, Barbara Albrecht-Küpper, Mihai Gheorghiade, Adriaan A Voors, Michael van der Laan, Hani N Sabbah
Adenosine exerts a variety of physiological effects by binding to cell surface G-protein-coupled receptor subtypes, namely, A1, A2a, A2b, and A3. The central physiological role of adenosine is to preclude tissue injury and promote repair in response to stress. In the heart, adenosine acts as a cytoprotective modulator, linking cardiac function to metabolic demand predominantly via activation of adenosine A1 receptors (A1Rs), which leads to inhibition of adenylate cyclase activity, modulation of protein kinase C, and opening of ATP-sensitive potassium channels...
October 22, 2016: Handbook of Experimental Pharmacology
Shigemiki Omiya, Yosuke Omori, Manabu Taneike, Andrea Protti, Osamu Yamaguchi, Shizuo Akira, Ajay M Shah, Kazuhiko Nishida, Kinya Otsu
We have reported that the Toll-like receptor 9 (TLR9) signaling pathway plays an important role in the development of pressure overload-induced inflammatory responses and heart failure. However, its role in cardiac remodeling after myocardial infarction has not been elucidated.TLR9-deficient and control C57Bl/6 wild-type mice were subjected to left coronary artery ligation. The survival rate 14 days post-operation was significantly lower in TLR9-deficient mice than that in wild-type mice with evidence of cardiac rupture in all dead mice...
October 21, 2016: American Journal of Physiology. Heart and Circulatory Physiology
Milad C El Hajj, Van K Ninh, Elia C El Hajj, Jessica M Bradley, Jason D Gardner
We have previously demonstrated the cardioprotective effects of ovarian hormones against adverse ventricular remodeling imposed by chronic volume overload. Here, we assess the estrogen receptor dependence of this cardioprotection. Four groups of female rats were studied: sham-operated (SHAM), volume overloaded (ACF), SHAM treated with estrogen receptor antagonist, ICI 182,780 (SHAM+ICI), and ACF treated with ICI. Cardiac function was assessed temporally using echocardiogram and tissue samples were collected at 5 days and 6 weeks post-surgery...
October 21, 2016: American Journal of Physiology. Heart and Circulatory Physiology
Julia O Reynolds, Ann P Quick, Qiongling Wang, David L Beavers, Leonne E Philippen, Jordan Showell, Giselle Barreto-Torres, Donna J Thuerauf, Shirin Doroudgar, Christopher C Glembotski, Xander H T Wehrens
BACKGROUND: Junctophilin-2 (JPH2) is the primary structural protein for the coupling of transverse (T)-tubule associated cardiac L-type Ca channels and type-2 ryanodine receptors on the sarcoplasmic reticulum within junctional membrane complexes (JMCs) in cardiomyocytes. Effective signaling between these channels ensures adequate Ca-induced Ca release required for normal cardiac contractility. Disruption of JMC subcellular domains, a common feature of failing hearts, has been attributed to JPH2 downregulation...
October 8, 2016: International Journal of Cardiology
Rosita Zakeri, Gilles Moulay, Qiang Chai, Ozgur Ogut, Saad Hussain, Hiroyuki Takahama, Tong Lu, Xiao-Li Wang, Wolfgang A Linke, Hon-Chi Lee, Margaret M Redfield
BACKGROUND: Left atrial (LA) compliance and contractility influence left ventricular stroke volume. We hypothesized that diminished LA compliance and contractile function occur early during the development of heart failure with preserved ejection fraction (HFpEF) and impair overall cardiac performance. METHODS AND RESULTS: Cardiac magnetic resonance imaging, echocardiography, left ventricular and LA pressure-volume studies, and tissue analyses were performed in a model of early HFpEF (elderly dogs, renal wrap-induced hypertension, exogenous aldosterone; n=9) and young control dogs (sham surgery; n=13)...
October 2016: Circulation. Heart Failure
Zhanna Kobalava
The burden of cardiovascular diseases (CVD) in general and heart failure (HF) in particular continues to increase worldwide. CVD are major contributors to death and morbidity and recognized as important drivers of healthcare expenditure. Chronic overactivity of the renin-angiotensin-aldosterone system (RAAS) plays a key role in human hypertension and HF pathophysiology. RAAS is fundamental in the overall regulation of cardiovascular homeostasis through the actions of hormones, which regulate vascular tone, and specifically blood pressure through vasoconstriction and renal sodium and water retention...
September 2016: Journal of Hypertension
Peter F Davies, Elisabetta Manduchi, Christian J Stoeckert, Yi-Zhou Jiang
Hemodynamics creates a constantly changing physical and chemical environment to which the arterial endothelium is exquisitely sensitive. Biomechanical stresses are intrinsic to blood flow characteristics and blood pressure and therefore are important considerations in hypertension. Near branching anatomical sites in arteries, blood flow separates from the main flow to undergo complex multi-directional characteristics for a part of each cardiac cycle (collectively referred to as disturbed flow). Atherosclerosis and aneurysmal pathology develop preferentially at disturbed flow locations, particularly when an additional cardiovascular risk factor such as hypercholesterolemia or high blood pressure are present...
September 2016: Journal of Hypertension
ByungSu Yoo
Hypertension is the most common risk factor for systolic and diastolic heart failure. Based on population-attributable risks, hypertension has the greatest impact on the development of heart failure, accounting for 39% of HF events in men and 59% in women. Higher blood pressure, longer duration of hypertension and older age are associated with higher incidence of heart failure however, long term control of hypertension reduces the risk of heart failure. Thus current guideline pointed the hypertension as the single most important modifiable risk factor for heart failure...
September 2016: Journal of Hypertension
V A Nevzorova, E A Kochetkova, L G Ugai, Yu V Maistrovskaya, E A Khludeeva
AIM: To define the role of circulating biomarkers for the metabolism of collagen and intercellular substance and vascular remodeling in the development of osteoporosis (OP) in idiopathic pulmonary arterial hypertension (IPAH). MATERIAL AND METHODS: Functional hemodynamic parameters, bone mineral density (BMD) in the lumbar spine and femoral neck and the serum levels of matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), MMP-9/TIMP-1 complex, C-terminal telopeptide of collagen type 1 (CITP), and endothelin-1 (ET-1) were determined in 27 high-risk IPAH patients and 30 healthy volunteers...
2016: Terapevticheskiĭ Arkhiv
Shweta R Motiwala, Hanna K Gaggin
Left ventricular remodeling appears to be a critical link between cardiac injury and the development and progression of heart failure with reduced ejection fraction (HFrEF). Several drug and device therapies that modify and reverse the remodeling process in patients with HFrEF are closely associated with improvement in clinical outcomes. Reverse remodeling, including partial or complete recovery of systolic function and structure, is possible but its determinants are incompletely understood. Methods to predict reverse remodeling in response to therapy are not well defined...
October 10, 2016: Current Heart Failure Reports
Christian Faul
Fibroblast growth factors (FGF) are mitogenic signal mediators that induce cell proliferation and survival. Although cardiac myocytes are post-mitotic, they have been shown to be able to respond to local and circulating FGFs. While precise molecular mechanisms are not well characterized, some FGF family members have been shown to induce cardiac remodeling under physiologic conditions by mediating hypertrophic growth in cardiac myocytes and by promoting angiogenesis, both events leading to increased cardiac function and output...
October 7, 2016: Bone
Saro H Armenian, Melissa M Hudson, Ming Hui Chen, Steven D Colan, Lanie Lindenfeld, George Mills, Aida Siyahian, Sarah Gelehrter, Ha Dang, Wendy Hein, Daniel M Green, Leslie L Robison, F Lennie Wong, Pamela S Douglas, Smita Bhatia
BACKGROUND: Anthracyclines are widely used in the treatment of childhood cancer. One of the well-recognized side-effects of anthracycline therapy is dose-dependent cardiomyopathy that may progress to heart failure (HF) years after completion of cancer-directed therapy. This study will evaluate the efficacy of low-dose beta-blocker (carvedilol) for HF risk reduction in childhood cancer survivors at highest risk for HF. The proposed intervention has the potential to significantly reduce chronic cardiac injury via interruption of neurohormonal systems responsible for left ventricular (LV) remodeling, resulting in improved cardiac function and decreased risk of HF...
October 4, 2016: BMC Cardiovascular Disorders
Shivika S Gupta, Matthew R Zeglinski, Sunil G Rattan, Natalie M Landry, Saeid Ghavami, Jeffrey T Wigle, Thomas Klonisch, Andrew J Halayko, Ian M C Dixon
The incidence of heart failure with concomitant cardiac fibrosis is very high in developed countries. Fibroblast activation in heart is causal to cardiac fibrosis as they convert to hypersynthetic cardiac myofibroblasts. There is no known treatment for cardiac fibrosis. Myofibroblasts contribute to the inappropriate remodeling of the myocardial interstitium, which leads to reduced cardiac function and ultimately heart failure. Elevated levels of autophagy have been linked to stress-induced ventricular remodeling and other cardiac diseases...
October 1, 2016: Oncotarget
Yuan Yuan, Ling Yan, Qing-Qing Wu, Heng Zhou, Ya-Ge Jin, Zhou-Yan Bian, Wei Deng, Zheng Yang, Di-Fei Shen, Xiao-Feng Zeng, Sha-Sha Wang, Hongliang Li, Qi-Zhu Tang
Identifying the key factor involved in cardiac remodeling is critically important for developing novel strategies to protect against heart failure. Here, the role of Mnk1 (mitogen-activated protein kinase-interacting kinase 1) in cardiac remodeling was clarified. Cardiac remodeling was induced by transverse aortic constriction in Mnk1-knockout mice and their wild-type control mice. After 4 weeks of transverse aortic constriction, Mnk1-knockout mice developed exaggerated cardiac hypertrophy, fibrosis, dysfunction, and cardiomyocyte apoptosis and showed increased ERK1/2 (extracellular signal-regulated kinase 1/2) activation along with reduced sprouty2 expression...
October 3, 2016: Hypertension
Antoine Heni Chaanine, Erik Kohlbrenner, Scott I Gamb, Adam J Guenzel, Katherine A Klaus, Ahmed U Fayyaz, K Sreekumaran Nair, Roger J Hajjar, Margaret M Redfield
The Forkhead box O3a (FOXO3a) transcription factor has been shown to regulate glucose metabolism, muscle atrophy and cell death in post-mitotic cells. Its role in regulating mitochondrial and myocardial function is not well studied. Based on previous work, we hypothesized that FOXO3a, through BNIP3, modulates mitochondrial morphology and function in HF. We modulated the FOXO3a-BNIP3 pathway in normal and phenylephrine (PE) stressed adult cardiac myocytes (ACM) in vitro and developed a cardiotropic adeno-associated virus serotype 9 encoding dominant-negative FOXO3a (AAV9...
September 30, 2016: American Journal of Physiology. Heart and Circulatory Physiology
Subendu Sarkar, Seema Chopra, Manoj Kumar Rohit, Dibyajyoti Banerjee, Anuradha Chakraborti
Rheumatic heart disease (RHD) remains a major cause of cardiac related mortality and morbidity in the developing countries due to poor diagnosis and lack of proper therapeutics. The definite reason of heart valve injury during RHD is poorly understood. Valvular endothelial cells play an important role in pathogenesis of different cardiovascular diseases. Besides, the regulation of vitamin D (calciferol) and VEGF (vascular endothelial growth factor) results in the functional changes in endothelial cells. However, the crosstalk between vitamin D and VEGF in the pathogenesis of RHD is not yet unfurled...
October 2016: Medical Hypotheses
Shashi Kumar Gupta, Ariana Foinquinos, Sabrina Thum, Janet Remke, Karina Zimmer, Christophe Bauters, Pascal de Groote, Reinier A Boon, Leon J de Windt, Sebastian Preissl, Lutz Hein, Sandor Batkai, Florence Pinet, Thomas Thum
BACKGROUND: Aging populations show higher incidences of myocardial infarction (MI) and heart failure (HF). Cardiac remodeling post-MI leads to progressive impaired cardiac function caused by a disarray of several processes including derailed autophagy. Microribonucleic acids (miRNAs) are known to be key players in cardiovascular disease but their involvement in cardiac autophagy and aging is not well understood. OBJECTIVES: This study sought to identify new miRNA candidates that regulate cardiac autophagy and aging...
October 4, 2016: Journal of the American College of Cardiology
Zhe Tian, Keishi Miyata, Tsuyoshi Kadomatsu, Haruki Horiguchi, Hiroyuki Fukushima, Shugo Tohyama, Yoshihiro Ujihara, Takahiro Okumura, Satoshi Yamaguchi, Jiabin Zhao, Motoyoshi Endo, Jun Morinaga, Michio Sato, Taichi Sugizaki, Shunshun Zhu, Kazutoyo Terada, Hisashi Sakaguchi, Yoshihiro Komohara, Motohiro Takeya, Naoki Takeda, Kimi Araki, Ichiro Manabe, Keiichi Fukuda, Kinya Otsu, Jun Wada, Toyoaki Murohara, Satoshi Mohri, Jun K Yamashita, Motoaki Sano, Yuichi Oike
A cardioprotective response that alters ventricular contractility or promotes cardiomyocyte enlargement occurs with increased workload in conditions such as hypertension. When that response is excessive, pathological cardiac remodelling occurs, which can progress to heart failure, a leading cause of death worldwide. Mechanisms underlying this response are not fully understood. Here, we report that expression of angiopoietin-like protein 2 (ANGPTL2) increases in pathologically-remodeled hearts of mice and humans, while decreased cardiac ANGPTL2 expression occurs in physiological cardiac remodelling induced by endurance training in mice...
September 28, 2016: Nature Communications
Rui-Fang Li, Shan-Shan Cao, Wei-Jin Fang, Ying Song, Xue-Ting Luo, Hong-Yun Wang, Jian-Gang Wang
Recent studies indicate that histone deacetylases (HDACs) activity is associated with the development and progression of cardiac hypertrophy. In this study, we investigated the effects of a HDACs inhibitor, valproic acid sodium (VPA), on cardiac remodeling and the differential expression of HDACs in left ventricles (LVs) of renovascular hypertensive rats. Renovascular hypertension was induced in rats by the two-kidney two-clip (2K2C) method. Cardiac remodeling, heart function and the differential expression of HDACs were examined at different weeks after 2K2C operation...
September 27, 2016: Pharmacology
Marco Matteucci, Valentina Casieri, Khatia Gabisonia, Giovanni Donato Aquaro, Silvia Agostini, Giuseppe Pollio, Daniela Diamanti, Marco Rossi, Massimiliano Travagli, Valentina Porcari, Fabio A Recchia, Vincenzo Lionetti
AIMS: Combined magnetic resonance imaging (MRI) of molecular and morpho-functional changes might prove highly valuable for the elucidation of pathological processes involved in the development of cardiac diseases. Our aim was to test a novel MRI reporter gene for in vivo assessment of the canonical Wnt/β-catenin/TCF pathway activation, an important regulator of post-ischemic cardiac remodeling. METHODS AND RESULTS: We designed and developed a chimeric construct encoding for both of iron-binding human ferritin heavy chain (hFTH) controlled by the β-catenin-responsive TCF/Lef promoter and constitutively expressed green fluorescent protein (GFP)...
September 26, 2016: Cardiovascular Research
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