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Cardiac apoptosis

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https://www.readbyqxmd.com/read/27936461/pterostilbene-protects-against-myocardial-ischemia-reperfusion-injury-via-suppressing-oxidative-nitrative-stress-and-inflammatory-response
#1
Zhaoxia Yu, Shaohua Wang, Xiangyang Zhang, Ying Li, Qiang Zhao, Tao Liu
Recent studies have shown that pterostilbene (Pte) confers protection against myocardial ischemia/reperfusion injury. The oxidative/nitrative stress and inflammation induce injury after myocardial ischemia/reperfusion. The present study was designed to evaluate whether treatment with Pte attenuates oxidative/nitrative stress and inflammation in myocardial ischemia/reperfusion (MI/R). Rats were subjected to 30min of myocardial ischemia and 3h of reperfusion, and the rats were administered with vehicle or Pte...
December 6, 2016: International Immunopharmacology
https://www.readbyqxmd.com/read/27936134/correction-early-fluid-resuscitation-by-lactated-ringer-s-solution-alleviate-the-cardiac-apoptosis-in-rats-with-trauma-hemorrhagic-shock
#2
Kuan-Ho Lin, Chien-Liang Liu, Wei-Wen Kuo, Catherine Reena Paul, Wei-Kung Chen, Su-Ying Wen, Cecilia Hsuan Day, Hsi-Chin Wu, Vijaya Padma Viswanadha, Chih-Yang Huang
[This corrects the article DOI: 10.1371/journal.pone.0165406.].
2016: PloS One
https://www.readbyqxmd.com/read/27933370/doxorubicin-induced-chronic-dilated-cardiomyopathy-the-apoptosis-hypothesis-revisited
#3
REVIEW
Cynthia Kankeu, Kylie Clarke, Egle Passante, Heinrich J Huber
The chemotherapeutic agent doxorubicin (DOX) has significantly increased survival rates of pediatric and adult cancer patients. However, 10% of pediatric cancer survivors will 10-20 years later develop severe dilated cardiomyopathy (DCM), whereby the exact molecular mechanisms of disease progression after this long latency time remain puzzling. We here revisit the hypothesis that elevated apoptosis signaling or its increased likelihood after DOX exposure can lead to an impairment of cardiac function and cause a cardiac dilation...
December 8, 2016: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/27932994/comparative-mrna-and-microrna-profiling-during-acute-myocardial-infarction-induced-by-coronary-occlusion-and-ablation-radio-frequency-currents
#4
Eduardo T Santana, Regiane Dos Santos Feliciano, Andrey J Serra, Eduardo Brigidio, Ednei L Antonio, Paulo J F Tucci, Lubov Nathanson, Mariana Morris, José A Silva
The ligation of the left anterior descending coronary artery is the most commonly used experimental model to induce myocardial infarction (MI) in rodents. A high mortality in the acute phase and the heterogeneity of the size of the MI obtained are drawbacks recognized in this model. In an attempt to solve the problem, our group recently developed a new MI experimental model which is based on application of myocardial ablation radio-frequency currents (AB-RF) that yielded MI with homogeneous sizes and significantly reduce acute mortality...
2016: Frontiers in Physiology
https://www.readbyqxmd.com/read/27932075/non-enzymatic-oxidized-metabolite-of-dha-4-rs-4-f4t-neuroprostane-protects-the-heart-against-reperfusion-injury
#5
Jérôme Roy, Jérémy Fauconnier, Camille Oger, Charlotte Farah, Claire Angebault-Prouteau, Jérôme Thireau, Patrice Bideaux, Valérie Scheuermann, Valérie Bultel-Poncé, Marie Demion, Jean-Marie Galano, Thierry Durand, Jetty Chung-Yung Lee, Jean-Yves Le Guennec
Acute myocardial infarction leads to an increase in oxidative stress and lipid peroxidation. 4(RS)-4-F4t-Neuroprostane (4-F4t-NeuroP) is a mediator produced by non-enzymatic free radical peroxidation of the cardioprotective polyunsaturated fatty acid, docosahexaenoic acid (DHA). In this study, we investigated whether intra-cardiac delivery of 4-F4t-NeuroP (0.03mg/kg) prior to occlusion (ischemia) prevents and protects rat myocardium from reperfusion damages. Using a rat model of ischemic-reperfusion (I/R), we showed that intra-cardiac infusion of 4-F4t-NeuroP significantly decreased infarct size following reperfusion (-27%) and also reduced ventricular arrhythmia score considerably during reperfusion (-41%)...
December 5, 2016: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/27931027/anthracycline-induced-cardiotoxicity-in-young-cancer-patients-the-role-of-carnitine
#6
Saro H Armenian
While the increased rates of survival in childhood cancers have increased progressively in recent decades, many childhood cancer survivors will have at least one chronic health condition within 40 years of age. In this regard, cardiovascular complications have emerged as a leading cause of long-term morbidity and mortality in long-term survivors of childhood cancer, likely due to exposure to anthracycline chemotherapy, and outcomes in patients with anthracycline-related cardiomyopathy remain poor. Some progress has been made in understanding the mechanisms at the basis of anthracycline-related cardiomyopathy, which appear to involve generation of reactive oxygen species, leading to mitochondrial dysfunction, followed by myocyte apoptosis and maladaptive left ventricular remodeling...
December 9, 2016: Annals of Nutrition & Metabolism
https://www.readbyqxmd.com/read/27930699/estrogen-protects-the-female-heart-from-ischemia-reperfusion-injury-through-manganese-superoxide-dismutase-phosphorylation-by-mitochondrial-p38%C3%AE-at-threonine-79-and-serine-106
#7
Tao Luo, Han Liu, Jin Kyung Kim
A collective body of evidence indicates that estrogen protects the heart from myocardial ischemia/reperfusion (I/R) injury, but the underlying mechanism remains incompletely understood. We have previously delineated a novel mechanism of how 17β-estradiol (E2) protects cultured neonatal rat cardiomyocytes from hypoxia/reoxygenation (H/R) by identifying a functionally active mitochondrial pool of p38β and E2-driven upregulation of manganese superoxide dismutase (MnSOD) activity via p38β, leading to the suppression of reactive oxygen species (ROS) and apoptosis...
2016: PloS One
https://www.readbyqxmd.com/read/27929425/the-coexistence-of-hypertension-and-ovariectomy-additively-increases-cardiac-apoptosis
#8
Yi-Yuan Lin, Yu-Jung Cheng, Jun Hu, Li-Xi Chu, Woei-Cherng Shyu, Chung-Lan Kao, Tzer-Bin Lin, Chia-Hua Kuo, Ai-Lun Yang, Shin-Da Lee
To investigate whether the coexistence of hypertension and ovariectomy will increase cardiac Fas receptor and mitochondrial-dependent apoptotic pathways, histopathological analysis, the TUNEL assay and Western blotting were performed on the excised hearts from three groups of female spontaneously hypertensive rats (SHR), which were divided into a sham-operated group (SHR-Sham), bilaterally ovariectomized group (SHR-OVX) and normotensive Wistar Kyoto rats (WKY). Compared with the WKY group, the SHR-Sham group exhibited decreased protein levels of ERα, ERβ, p-Akt/Akt, Bcl-2, Bcl-xL and p-Bad and decreased further in the SHR-OVX group, as well as protein levels of t-Bid, Bak, Bad, Bax, cytochrome c, activated caspase-9 and activated caspase-3 (mitochondria-dependent apoptosis) increased in the SHR-Sham group and increased further in the SHR-OVX group...
December 6, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27929137/inhibition-of-pkr-protects-against-h2o2-induced-injury-on-neonatal-cardiac-myocytes-by-attenuating-apoptosis-and-inflammation
#9
Yongyi Wang, Min Men, Bo Xie, Jianggui Shan, Chengxi Wang, Jidong Liu, Hui Zheng, Wengang Yang, Song Xue, Changfa Guo
Reactive oxygenation species (ROS) generated from reperfusion results in cardiac injury through apoptosis and inflammation, while PKR has the ability to promote apoptosis and inflammation. The aim of the study was to investigate whether PKR is involved in hydrogen peroxide (H2O2) induced neonatal cardiac myocytes (NCM) injury. In our study, NCM, when exposed to H2O2, resulted in persistent activation of PKR due to NCM endogenous RNA. Inhibition of PKR by 2-aminopurine (2-AP) or siRNA protected against H2O2 induced apoptosis and injury...
December 8, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27924873/cardiac-specific-overexpression-of-mitochondrial-omi-htra2-induces-myocardial-apoptosis-and-cardiac-dysfunction
#10
Ke Wang, Yuexing Yuan, Xin Liu, Wayne Bond Lau, Lin Zuo, Xiaoliang Wang, Lu Ma, Kun Jiao, Jianyu Shang, Wen Wang, Xinliang Ma, Huirong Liu
Myocardial apoptosis is a significant problem underlying ischemic heart disease. We previously reported significantly elevated expression of cytoplasmic Omi/HtrA2, triggers cardiomyocytes apoptosis. However, whether increased Omi/HtrA2 within mitochondria itself influences myocardial survival in vivo is unknown. We aim to observe the effects of mitochondria-specific, not cytoplasmic, Omi/HtrA2 on myocardial apoptosis and cardiac function. Transgenic mice overexpressing cardiac-specific mitochondrial Omi/HtrA2 were generated and they had increased myocardial apoptosis, decreased systolic and diastolic function, and decreased left ventricular remodeling...
December 7, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27924067/chronic-intermittent-hypoxia-induces-cardiac-inflammation-and-dysfunction-in-a-rat-obstructive-sleep-apnea-model
#11
Qin Wei, Yeping Bian, Fuchao Yu, Qiang Zhang, Guanghao Zhang, Yang Li, Songsong Song, Xiaomei Ren, Jiayi Tong
Chronic intermittent hypoxia is considered to play an important role in cardiovascular pathogenesis during the development of obstructive sleep apnea (OSA). We used a well-described OSA rat model induced with simultaneous intermittent hypoxia. Male Sprague Dawley rats were individually placed into plexiglass chambers with air pressure and components were electronically controlled. The rats were exposed to intermittent hypoxia 8 hours daily for 5 weeks. The changes of cardiac structure and function were examined by ultrasound...
November 2016: Journal of Biomedical Research
https://www.readbyqxmd.com/read/27922664/expression-of-bcl-2-and-micrornas-in-cardiac-tissues-of-patients-with-dilated-cardiomyopathy
#12
Yong Wang, Min Li, Li Xu, Ju Liu, Dong Wang, Quan Li, Lili Wang, Peijie Li, Shanliang Chen, Tianqi Liu
Dilated cardiomyopathy (DCM) is associated with sudden cardiac death and heart failure, resulting in a significant medical burden. The mechanisms underlying the pathogenesis of DCM remain elusive. In the present study, human cardiac tissues from patients with DCM and healthy donors were collected and their pathology was examined. The expression levels of apoptosis regulator Bcl-2 and fibrosis-associated microRNAs were also evaluated. Extensive myocardial fibrosis and apoptosis in DCM cardiac tissues was observed...
December 2, 2016: Molecular Medicine Reports
https://www.readbyqxmd.com/read/27919929/interleukin-37-and-dendritic-cells-treated-with-interleukin-37-plus-troponin-i-ameliorate-cardiac-remodeling-after-myocardial-infarction
#13
Ruirui Zhu, Haitao Sun, Kunwu Yu, Yucheng Zhong, Huairui Shi, Yuzhen Wei, Xin Su, Wenbin Xu, Quan Luo, Fangyuan Zhang, Zhengfeng Zhu, Kai Meng, Xiaoqi Zhao, Yuzhou Liu, Yi Mao, Peng Cheng, Xiaobo Mao, Qiutang Zeng
BACKGROUND: Excessive immune-mediated inflammatory reactions play a deleterious role in postinfarction ventricular remodeling. Interleukin-37 (IL-37) emerges as an inhibitor of both innate and adaptive immunity. However, the exact role of IL-37 and IL-37 plus troponin I (TnI)-treated dendritic cells (DCs) in ventricular remodeling after myocardial infarction (MI) remains elusive. METHODS AND RESULTS: MI was induced by permanent ligation of the left anterior descending artery...
December 5, 2016: Journal of the American Heart Association
https://www.readbyqxmd.com/read/27916680/the-role-of-micrornas-in-heart-failure
#14
REVIEW
Hongjiang Wang, Jun Cai
MicroRNAs are small non-coding RNA molecules that regulate gene expression by inhibiting mRNA translation and/or inducing mRNA degradation. In the past decade, many in vitro and in vivo studies have explored the involvement of microRNAs in various cardiovascular diseases. In this paper, studies focused upon the target genes and functionality of miRNAs in the pathophysiological processes of heart failure are reviewed. The selected miRNAs are categorized according to the biological relevance of their target genes in relation to four cardiovascular pathologies, namely angiogenesis, cardiac hypertrophy, fibrosis and apoptosis...
December 1, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27916558/role-of-carvacrol-in-cardioprotection-against-myocardial-ischemia-reperfusion-injury-in-rats-through-activation-of-mapk-erk-and-akt-enos-signaling-pathways
#15
Yunping Chen, Lina Ba, Wei Huang, Yan Liu, Hao Pan, E Mingyao, Pilong Shi, Ye Wang, Shuzhi Li, Hanping Qi, Hongli Sun, Yonggang Cao
Carvacrol (CAR) is a compound isolated from some essential oils, many studies have demonstrated its therapeutic potential on different diseases. This study aims to evaluate the protective effect of CAR against myocardial ischemia/reperfusion (I/R) injury in rats. Male adult rats underwent ligation of the left anterior descending coronary artery (LAD) in I/R models. Rats were treated with CAR after LAD. The levels of I/R- induced infarct size, cardiomyocyte apoptosis and cardiac functional impairment were examined...
December 1, 2016: European Journal of Pharmacology
https://www.readbyqxmd.com/read/27913284/cardiac-proteasome-functional-insufficiency-plays-a-pathogenic-role-in-diabetic-cardiomyopathy
#16
Jie Li, Wenxia Ma, Guihua Yue, Yaoliang Tang, Il-Man Kim, Neal L Weintraub, Xuejun Wang, Huabo Su
BACKGROUND: Diabetic cardiomyopathy is a major risk factor in diabetic patients but its pathogenesis remains poorly understood. The ubiquitin-proteasome system (UPS) facilitates protein quality control by degrading unnecessary and damaged proteins in eukaryotic cells, and dysfunction of UPS is implicated in various cardiac diseases. However, the overall functional status of the UPS and its pathophysiological role in diabetic cardiomyopathy have not been determined. METHODS AND RESULTS: Type I diabetes was induced in wild-type and transgenic mice expressing a UPS functional reporter (GFPdgn) by injections of streptozotocin (STZ)...
November 29, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27913127/co-assembly-of-doxorubicin-and-curcumin-targeted-micelles-for-synergistic-delivery-and-improving-anti-tumor-efficacy
#17
Wenzhuan Ma, Qiang Guo, Ying Li, Xiaohui Wang, Jinling Wang, Pengfei Tu
Chemotherapeutic drugs have a series of limitations in anti-tumor treatment, mainly including multidrug resistance (MDR) and serious adverse reactions. Co-delivery system with two or more synergistic therapeutic drugs is an effective strategy to settle these limitations. In this study, active tumor-targeted co-delivery micelles (DOX+Cur)-PMs, with two synergistic drugs of a therapeutic drug of doxorubicin (DOX) and a chemosensitizer of curcumin (Cur) co-encapsulated into hyaluronic acid-vitamin E succinate (HA-VES) graft copolymer, were prepared and delivered simultaneously into tumor cells for improving therapeutic effects of DOX...
November 29, 2016: European Journal of Pharmaceutics and Biopharmaceutics
https://www.readbyqxmd.com/read/27911441/sirt1-protects-the-heart-from-er-stress-induced-cell-death-through-eif2%C3%AE-deacetylation
#18
Alexandre Prola, Julie Pires Da Silva, Arnaud Guilbert, Lola Lecru, Jérôme Piquereau, Maxance Ribeiro, Philippe Mateo, Mélanie Gressette, Dominique Fortin, Céline Boursier, Cindy Gallerne, Anaïs Caillard, Jane-Lise Samuel, Hélène François, David A Sinclair, Pierre Eid, Renée Ventura-Clapier, Anne Garnier, Christophe Lemaire
Over the past decade, endoplasmic reticulum (ER) stress has emerged as an important mechanism involved in the pathogenesis of cardiovascular diseases including heart failure. Cardiac therapy based on ER stress modulation is viewed as a promising avenue toward effective therapies for the diseased heart. Here, we tested whether sirtuin-1 (SIRT1), a NAD(+)-dependent deacetylase, participates in modulating ER stress response in the heart. Using cardiomyocytes and adult-inducible SIRT1 knockout mice, we demonstrate that SIRT1 inhibition or deficiency increases ER stress-induced cardiac injury, whereas activation of SIRT1 by the SIRT1-activating compound STAC-3 is protective...
December 2, 2016: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27909014/sodium-4-phenylbutyrate-attenuates-myocardial-reperfusion-injury-by-reducing-the-unfolded-protein-response
#19
Osamu Takatori, Soichiro Usui, Masaki Okajima, Shuichi Kaneko, Hiroshi Ootsuji, Shin-Ichiro Takashima, Daisuke Kobayashi, Hisayoshi Murai, Hiroshi Furusho, Masayuki Takamura
BACKGROUND: The unfolded protein response (UPR) plays a pivotal role in ischemia-reperfusion (I/R) injury in various organs such as heart, brain, and liver. Sodium 4-phenylbutyrate (PBA) reportedly acts as a chemical chaperone that reduces UPR. In the present study, we evaluated the effect of PBA on reducing the UPR and protecting against myocardial I/R injury in mice. METHODS: Male C57BL/6 mice were subjected to 30-minute myocardial I/R, and were treated with phosphate-buffered saline (as a vehicle) or PBA...
December 1, 2016: Journal of Cardiovascular Pharmacology and Therapeutics
https://www.readbyqxmd.com/read/27904669/astragaloside-iv-enhances-cardioprotection-of-remote-ischemic-conditioning-after-acute-myocardial-infarction-in-rats
#20
Songyi Cheng, Peng Yu, Li Yang, Haibo Shi, Anxia He, Hanyu Chen, Jie Han, Liang Xie, Jiandong Chen, Xiaohu Chen
BACKGROUND: Remote ischemic conditioning (RIC) has been shown to be a practical method for protecting the heart from ischemic/reperfusion (I/R) injury. In the present study, we investigated whether or not the combination of RIC and Astragaloside IV (AS-IV) could improve cardioprotection against acute myocardial infarction (AMI)-induced heart failure (HF) when compared with individual treatments. MATERIAL AND METHODS: A rat model of AMI was established via permanent ligation of the left anterior descending coronary artery (LAD)...
2016: American Journal of Translational Research
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