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stress and cardiac death

C Manghani, A Gupta, V Tripathi, V Rani
Cardiomyopathy and associated heart failure continues to be one of the most severe complications that threaten a large population. Curcumin, one of the three curcuminoids of the spice turmeric, is very well known for a multitude of health benefits and functions. Norepinephrine (NE), a catecholamine and also a stress hormone may cause the cardiomyocytes to develop increased sensitivity to death with its increasing concentrations. In this study, we investigated the cardioprotective effect of curcumin in NE-induced cardiac apoptosis using several fluorescent and nonfluorescent microscopic techniques like DAPI, PI, Giemsa, PicroSirius and TUNEL...
October 25, 2016: Journal of Microscopy
Joseph B Fisher, Audrey Horst, Tina Wan, Min-Su Kim, John Auchampach, John Lough
Tat-interactive protein 60 (Tip60), encoded by the Kat5 gene, is a member of the MYST family of acetyltransferases. Cancer biology studies have shown that Tip60 induces the DNA damage response, apoptosis, and cell-cycle inhibition. Although Tip60 is expressed in the myocardium, its role in cardiomyocytes (CMs) is unclear. Earlier studies here showed that application of cardiac stress to globally targeted Kat5+/-haploinsufficient mice resulted in inhibition of apoptosis and activation of the CM cell-cycle, despite only modest reduction of Tip60 protein levels...
2016: PloS One
Yang Sun, Dajun Zhao, Yang Yang, Chao Gao, Xing Zhang, Zhiqiang Ma, Shuai Jiang, Lin Zhao, Wenhao Chen, Kai Ren, Wei Yi, Feng Gao
The underlying mechanisms of cardioprotection of adiponectin (APN) against ischemia/reperfusion (I/R) injury remain largely unknown. The present study aimed to investigate whether calreticulin (CRT) mediated APN's cardioprotection against I/R injury. We inhibited mice cardiac CRT expression via intra-myocardial injection of CRT SiRNA, performed transient LAD ligation, measured the cardiac function, apoptosis and oxidative stress to identify CRT's effects on cardioprotective actions of APN against I/R injury in vivo...
October 18, 2016: Apoptosis: An International Journal on Programmed Cell Death
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
Sang-Geon Cho, Zeenat Jabin, Ki Seong Park, Jahae Kim, Sae-Ryung Kang, Seong Young Kwon, Geum-Cheol Jeong, Minchul Song, Jong Sang Kim, Jae Yeong Cho, Hyun Kuk Kim, Ho-Chun Song, Jung-Joon Min, Hee-Seung Bom
PURPOSE: The aim of this study was to evaluate the prognostic value of additional evaluation of left ventricular mechanical dyssynchrony (LVMD) by gated myocardial perfusion single-photon emission computed tomography (GMPS) in patients with acute myocardial infarction (MI) and multivessel disease. METHODS: One hundred and nine acute MI patients with >50 % stenosis in at least one non-culprit artery who underwent GMPS within 2 weeks were enrolled. All patients underwent successful revascularization of the culprit arteries...
October 18, 2016: European Journal of Nuclear Medicine and Molecular Imaging
Murray Esler
The London physician and neuroanatomist Thomas Willis in the 17th century correctly attributed the source of emotions to the brain, not the heart as believed in antiquity. Contemporary research documents the phenomenon of "triggered" heart disease, when the autonomic nervous system control of the heart by the brain goes awry, producing heart disease of sudden onset, precipitated by acute emotional upheaval. This can take the form of, variously, cardiac arrhythmias, myocardial infarction, Takotsubo cardiomyopathy and sudden death...
October 14, 2016: Neuroscience and Biobehavioral Reviews
Jack H Boyd, Vedant S Pargaonkar, David H Scoville, Ian S Rogers, Takumi Kimura, Shigemitsu Tanaka, Ryotaro Yamada, Michael P Fischbein, Jennifer A Tremmel, Robert Scott Mitchell, Ingela Schnittger
BACKGROUND: Left anterior descending artery myocardial bridges (MBs) range from clinically insignificant incidental angiographic findings to a potential cause of sudden cardiac death. Within this spectrum, a group of patients with isolated, symptomatic, and hemodynamically significant MBs despite maximally tolerated medical therapy exist for whom the optimal treatment is controversial. We evaluated supraarterial myotomy, or surgical unroofing, of the left anterior descending MBs as an isolated procedure in these patients...
October 1, 2016: Annals of Thoracic Surgery
Pavlína Hašková, Hana Jansová, Jan Bureš, Miloslav Macháček, Anna Jirkovská, Katherine J Franz, Petra Kovaříková, Tomáš Šimůnek
Catecholamines may undergo iron-promoted oxidation resulting in formation of reactive intermediates (aminochromes) capable of redox cycling and reactive oxygen species (ROS) formation. Both of them induce oxidative stress resulting in cellular damage and death. Iron chelation has been recently shown as a suitable tool of cardioprotection with considerable potential to protect cardiac cells against catecholamine-induced cardiotoxicity. However, prolonged exposure of cells to classical chelators may interfere with physiological iron homeostasis...
October 12, 2016: Toxicology
Shangcheng Xu, Pei Wang, Huiliang Zhang, Guohua Gong, Nicolas Gutierrez Cortes, Weizhong Zhu, Yisang Yoon, Rong Tian, Wang Wang
Mitochondrial permeability transition pore (mPTP) is involved in cardiac dysfunction during chronic β-adrenergic receptor (β-AR) stimulation. The mechanism by which chronic β-AR stimulation leads to mPTP openings is elusive. Here, we show that chronic administration of isoproterenol (ISO) persistently increases the frequency of mPTP openings followed by mitochondrial damage and cardiac dysfunction. Mechanistically, this effect is mediated by phosphorylation of mitochondrial fission protein, dynamin-related protein 1 (Drp1), by Ca(2+)/calmodulin-dependent kinase II (CaMKII) at a serine 616 (S616) site...
October 14, 2016: Nature Communications
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
Shirin Doroudgar, Pearl Quijada, Mathias Konstandin, Kelli Ilves, Kathleen Broughton, Farid G Khalafalla, Alexandria Casillas, Kristine Nguyen, Natalie Gude, Haruhiro Toko, Luis Ornelas, Donna J Thuerauf, Christopher C Glembotski, Mark A Sussman, Mirko Völkers
BACKGROUND: Myocardial infarction is followed by cardiac dysfunction, cellular death, and ventricular remodeling, including tissue fibrosis. S100A4 protein plays multiple roles in cellular survival, and tissue fibrosis, but the relative role of the S100A4 in the myocardium after myocardial infarction is unknown. This study aims to investigate the role of S100A4 in myocardial remodeling and cardiac function following infarct damage. METHODS AND RESULTS: S100A4 expression is low in the adult myocardium, but significantly increased following myocardial infarction...
October 6, 2016: Journal of Molecular and Cellular Cardiology
Ruth E Bates, Mohamed Omer, Sahar S Abdelmoneim, Adelaide M Arruda-Olson, Christopher G Scott, Kent R Bailey, Robert B McCully, Patricia A Pellikka
OBJECTIVE: To evaluate the impact of screening stress testing for coronary artery disease in asymptomatic patients with diabetes in a community-based population. PATIENTS AND METHODS: This observational study included 3146 patients from Olmsted County, Minnesota, with no history of coronary artery disease or cardiac symptoms in whom diabetes was newly diagnosed from January 1, 1992, through December 31, 2008. With combined all-cause mortality and myocardial infarction as the primary outcome, weighted Cox proportional hazards regression was performed with screening stress testing within 2 years of diabetes diagnosis as the time-dependent covariate...
October 6, 2016: Mayo Clinic Proceedings
Jesper J Linde, Mathias Sørgaard, Jørgen T Kühl, Jens D Hove, Henning Kelbæk, Walter B Nielsen, Klaus F Kofoed
The prognostic implications of myocardial computed tomography perfusion (CTP) analyses are unknown. In this sub-study to the CATCH-trial we evaluate the ability of adenosine stress CTP findings to predict mid-term major adverse cardiac events (MACE). In 240 patients with acute-onset chest pain, yet normal electrocardiograms and troponins, a clinically blinded adenosine stress CTP scan was performed in addition to conventional diagnostic evaluation. A reversible perfusion defect (PD) was found in 38 patients (16 %) and during a median follow-up of 19 months (range 12-22 months) 25 patients (10 %) suffered a MACE (cardiac death, non-fatal myocardial infarction and revascularizations)...
October 7, 2016: International Journal of Cardiovascular Imaging
George J Dugbartey, Luke J Peppone, Inge A M de Graaf
Cisplatin is currently one of the most widely-used chemotherapeutic agents against various malignancies. Its clinical application is limited, however, by inherent renal and cardiac toxicities and other side effects, of which the underlying mechanisms are only partly understood. Experimental studies show cisplatin generates reactive oxygen species, which impair the cell's antioxidant defense system, causing oxidative stress and potentiating injury, thereby culminating in kidney and heart failure. Understanding the molecular mechanisms of cisplatin-induced renal and cardiac toxicities may allow clinicians to prevent or treat this problem better and may also provide a model for investigating drug-induced organ toxicity in general...
October 4, 2016: Toxicology
Yanfei Chen, Bryan W Tillman, Sung Kwon Cho, Tara D Richards, Amit D Tevar, Xinzhu Gu, William R Wagner, Youngjae Chun
Donation after cardiac death has been adopted to address the critical shortage of donor organs for transplant. Recovery of these organs is hindered by low blood flow that leads to permanent organ injury. We propose a novel approach to isolate the perfusion of the abdominal organs from the systemic malperfusion of the dying donor. We reasoned that this design could improve blood flow to organs without open surgery, while respecting the ethical principle that cardiac stress not be increased during organ recovery...
October 7, 2016: Journal of Medical Engineering & Technology
Małgorzata Kowalska, Krzysztof Kocot
Results of epidemiological studies suggest a significant impact of ambient particulate matter air pollution (PM10 and PM2,5) on the health of the population. Increased level of these pollutants is connected with increased rate of daily mortality and hospitalizations due to cardiovascular diseases. Among analyzed health effects, heart arrhythmias and stroke are mentioned most frequently. The aim of the study was to present the current knowledge of potential influence of the exposure to fine particulate matter on the presence of arrhythmias and strokes...
September 28, 2016: Postȩpy Higieny i Medycyny Doświadczalnej
Adam Kassan, Uyen Pham, Quynhmy Nguyen, Melissa E Reichelt, Eunbyul Cho, Piyush M Patel, David M Roth, Brian P Head, Hemal H Patel
Autophagy is a dynamic recycling process responsible for the breakdown of misfolded proteins and damaged organelles, providing nutrients and energy for cellular renovation and homeostasis. Loss of autophagy is associated with cardiovascular diseases. Caveolin-3 (Cav-3), a muscle-specific isoform, is a structural protein within caveolae and is critical to stress adaptation in the heart. Whether Cav-3 plays a role in regulating autophagy to modulate cardiac stress responses remains unknown. In the present study, we used HL-1 cells, a cardiac muscle cell line, with stable Cav-3 knockdown (Cav-3 KD) and Cav-3 over-expression (Cav-3 OE) to study the impact of Cav-3 in regulation of autophagy...
October 5, 2016: American Journal of Physiology. Cell Physiology
Xiaojian Zhang, Chengwu Shen, Shujun Zhai, Yukun Liu, Wen-Wei Yue, Li Han
Adrenergic β-blockers are drugs that bind to, but do not activate β-adrenergic receptors. Instead they block the actions of β-adrenergic agonists and are used for the treatment of various diseases such as cardiac arrhythmias, angina pectoris, myocardial infarction, hypertension, headache, migraines, stress, anxiety, prostate cancer, and heart failure. Several meta-analysis studies have shown that β-blockers improve the heart function and reduce the risks of cardiovascular events, rate of mortality, and sudden death through chronic heart failure (CHF) of patients...
October 2016: Experimental and Therapeutic Medicine
Kevin J Ashton, Melissa E Reichelt, S Jamal Mustafa, Bunyen Teng, Catherine Ledent, Lea M D Delbridge, Polly A Hofmann, R Ray Morrison, John P Headrick
Influences of adenosine 2A receptor (A2AR) activity on the cardiac transcriptome and genesis of endotoxemic myocarditis are unclear. We applied transcriptomic profiling (39 K Affymetrix arrays) to identify A2AR-sensitive molecules, revealed by receptor knockout (KO), in healthy and endotoxemic hearts. Baseline cardiac function was unaltered and only 37 A2AR-sensitive genes modified by A2AR KO (≥1.2-fold change, <5 % FDR); the five most induced are Mtr, Ppbp, Chac1, Ctsk and Cnpy2 and the five most repressed are Hp, Yipf4, Acta1, Cidec and Map3k2...
September 30, 2016: Purinergic Signalling
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
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