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Heart fibrosis

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https://www.readbyqxmd.com/read/27922664/expression-of-bcl-2-and-micrornas-in-cardiac-tissues-of-patients-with-dilated-cardiomyopathy
#1
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/27922176/dipeptidyl-peptidase-4-inhibitor-sitagliptin-reduces-inflammation-fibrosis-and-preserves-diastolic-function-in-a-rat-model-of-heart-failure-with-preserved-ejection-fraction
#2
Grazia Esposito, Donato Cappetta, Rosa Russo, Alessia Rivellino, Loreta Pia Ciuffreda, Fiorentina Roviezzo, Elena Piegari, L Liberato Berrino, Francesco Rossi, Antonella De Angelis, Konrad Urbanek
BACKGROUND AND PURPOSE: Heart failure with preserved ejection fraction (HFpEF) is a systemic syndrome driven by co-morbidities and its pathophysiology is poorly understood. Several studies suggesting that dipeptidyl peptidase 4 (DPP4) might be involved in the pathophysiology of heart failure prompted experimental and clinical investigations of DPP4 inhibitors on cardiovascular system. The aim of our study was to determine whether DPP4 inhibitor sitagliptin (SITA) affects the progression of HFpEF independently from the effects on glycaemia...
December 6, 2016: British Journal of Pharmacology
https://www.readbyqxmd.com/read/27920495/card9-as-a-potential-target-in-cardiovascular-disease
#3
REVIEW
Matthew R Peterson, Samantha E Haller, Jun Ren, Sreejayan Nair, Guanglong He
Systemic inflammation and localized macrophage infiltration have been implicated in cardiovascular pathologies, including coronary artery disease, carotid atherosclerosis, heart failure, obesity-associated heart dysfunction, and cardiac fibrosis. Inflammation induces macrophage infiltration and activation and release of cytokines and chemokines, causing tissue dysfunction by instigating a positive feedback loop that further propagates inflammation. Cytosolic adaptor caspase recruitment domain family, member 9 (CARD9) is a protein expressed primarily by dendritic cells, neutrophils, and macrophages, in which it mediates cytokine secretion...
2016: Drug Design, Development and Therapy
https://www.readbyqxmd.com/read/27920122/microrna-33-controls-adaptive-fibrotic-response-in-the-remodeling-heart-by-preserving-lipid-raft-cholesterol
#4
Masataka Nishiga, Takahiro Horie, Yasuhide Kuwabara, Kazuya Nagao, Osamu Baba, Tetsushi Nakao, Tomohiro Nishino, Daihiko Hakuno, Yasuhiro Nakashima, Hitoo Nishi, Fumiko Nakazeki, Yuya Ide, Satoshi Koyama, Masahiro Kimura, Ritsuko Hanada, Tomoyuki Nakamura, Tsukasa Inada, Koji Hasegawa, Simon J Conway, Toru Kita, Takeshi Kimura, Koh Ono
RATIONALE: Heart failure (HF) and atherosclerosis share the underlying mechanisms of chronic inflammation followed by fibrosis. A highly conserved microRNA (miR), miR-33 is considered as a potential therapeutic target for atherosclerosis because it regulates lipid metabolism and inflammation. However, the role of miR-33 in HF remains to be elucidated. OBJECTIVE: To clarify the role of miR-33 involved in HF. METHODS AND RESULTS: We first investigated the expression levels of miR-33a/b in human cardiac tissue samples with dilated cardiomyopathy...
December 5, 2016: Circulation Research
https://www.readbyqxmd.com/read/27919929/interleukin-37-and-dendritic-cells-treated-with-interleukin-37-plus-troponin-i-ameliorate-cardiac-remodeling-after-myocardial-infarction
#5
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/27919304/green-tea-extract-intake-during-lactation-modified-cardiac-macrophage-infiltration-and-amp-activated-protein-kinase-phosphorylation-in-weanling-rats-from-undernourished-mother-during-gestation-and-lactation
#6
E Matsumoto, S Kataoka, Y Mukai, M Sato, S Sato
Maternal dietary restriction is often associated with cardiovascular disease in offspring. The aim of this study was to investigate the effect of green tea extract (GTE) intake during lactation on macrophage infiltration, and activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK) and serine-threonine kinase Akt (Akt) in the hearts of weanlings exposed to maternal dietary protein restriction. Pregnant Wistar rats were fed control (C) or low-protein diets (LP) throughout gestation. Following delivery, the dams received a control or a GTE-containing control diet during lactation: control diet during gestation and lactation (CC), low-protein diet during gestation and lactation (LPC), low-protein diet during gestation and 0...
December 6, 2016: Journal of Developmental Origins of Health and Disease
https://www.readbyqxmd.com/read/27918308/cardiac-myofibroblast-engulfment-of-dead-cells-facilitates-recovery-after-myocardial-infarction
#7
Michio Nakaya, Kenji Watari, Mitsuru Tajima, Takeo Nakaya, Shoichi Matsuda, Hiroki Ohara, Hiroaki Nishihara, Hiroshi Yamaguchi, Akiko Hashimoto, Mitsuho Nishida, Akiomi Nagasaka, Yuma Horii, Hiroki Ono, Gentaro Iribe, Ryuji Inoue, Makoto Tsuda, Kazuhide Inoue, Akira Tanaka, Masahiko Kuroda, Shigekazu Nagata, Hitoshi Kurose
Myocardial infarction (MI) results in the generation of dead cells in the infarcted area. These cells are swiftly removed by phagocytes to minimize inflammation and limit expansion of the damaged area. However, the types of cells and molecules responsible for the engulfment of dead cells in the infarcted area remain largely unknown. In this study, we demonstrated that cardiac myofibroblasts, which execute tissue fibrosis by producing extracellular matrix proteins, efficiently engulf dead cells. Furthermore, we identified a population of cardiac myofibroblasts that appears in the heart after MI in humans and mice...
December 5, 2016: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/27917273/involvement-of-microrna-133-and-29-in-cardiac-disturbances-in-diabetic-ovariectomized-rats
#8
Parisa Habibi, Alireza Alihemmati, Mohammadreza Nasirzadeh, Hadi Yousefi, Mohammadrasoul Habibi, Nasser Ahmadiasl
OBJECTIVES: Menopause and diabetes obviously increase the risk of cardiovascular disease in women. The aims of the present study were to evaluate the effects of ovariectomy in type 2 diabetes on the histology and expression of miRNA-29, miRNA-133, IGF-1 and Bcl-2 genes and Bcl-2 protein and caspase 3 activity in the hearts of female rats. MATERIALS AND METHODS: Forty Female Wistar rats were divided into four groups: control, sham, ovariectomized (OVX), and ovariectomized with type 2 diabetes (OVX...
November 2016: Iranian Journal of Basic Medical Sciences
https://www.readbyqxmd.com/read/27916680/the-role-of-micrornas-in-heart-failure
#9
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/27916650/cardiac-oxidative-stress-in-diabetes-mechanisms-and-therapeutic-potential
#10
REVIEW
Alyssa Faria, Shanta J Persaud
Macrovascular complications of diabetes, including diabetic cardiovascular disease (CVD), occur through a number of hyperglycaemia-induced mechanisms that include generation of oxidative stress, accumulation of advanced glycation end-products (AGE) and activation of protein kinase C (PKC). Cardiac oxidative stress is associated with increased cardiac fibrosis and hypertrophy, and reduced cardiac performance and contractility, leading to severe cardiac dysfunction and potentially fatal cardiac events. It occurs under conditions of excessive synthesis of reactive oxygen species (ROS)...
December 1, 2016: Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/27912208/smad-nuclear-interacting-protein-1-acts-as-a-protective-regulator-of-pressure-overload-induced-pathological-cardiac-hypertrophy
#11
Yu-Yan Lu, Da-Chun Xu, Yi-Fan Zhao, Guo-Fu Zhu, Meng-Yun Zhu, Wei-Jing Liu, Xue-Jing Yu, Wei Chen, Zheng Liu, Ya-Wei Xu
BACKGROUND: Smad nuclear interacting protein 1 (SNIP1) plays a critical role in cell proliferation, transformation of embryonic fibroblasts, and immune regulation. However, the role of SNIP1 in cardiac hypertrophy remains unclear. METHODS AND RESULTS: Here we examined the role of SNIP1 in pressure overload-induced cardiac hypertrophy and its mechanisms. Our results demonstrated that SNIP1 expression was downregulated in human dilated cardiomyopathic hearts, aortic banding-induced mice hearts, and angiotensin II-treated cardiomyocytes...
October 26, 2016: Journal of the American Heart Association
https://www.readbyqxmd.com/read/27910055/selective-pressure-regulated-retroinfusion-for-gene-therapy-application-in-ischemic-heart-disease
#12
Rabea Hinkel, Christian Kupatt
Coronary heart disease is still the leading cause of death in industrialized nations. Even though revascularization strategies such as coronary artery bypass graft surgery, percutaneous coronary intervention and enhanced drug therapy significantly improved the outcome, about 30 % of patients develop chronic heart failure. Ischemic heart disease and heart failure are characterized by an adverse remodeling of the heart, featuring cardiomyocyte hypertrophy, increased fibrosis and capillary rarefaction. Therefore, gene therapeutic approaches for the treatment of heart failure, such as the modulating contractile function or therapeutic neovascularization, seem to be promising...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/27909478/cardiac-resynchronization-therapy-in-non-ischemic-cardiomyopathy
#13
REVIEW
Miriam Shanks Md PhD, Victoria Delgado Md PhD, Jeroen J Bax Md PhD
Cardiac resynchronization therapy (CRT) is an established therapy for heart failure patients who remain symptomatic despite optimal medical therapy, have reduced left ventricular ejection fraction (<35%) and wide QRS duration (>120 ms), preferably with left bundle branch block morphology. The response to CRT depends on the cardiac substrate: presence of correctable left ventricular mechanical dyssynchrony, presence of myocardial fibrosis (scar) and position of the left ventricular pacing lead. Patients with non-ischemic cardiomyopathy have shown higher response rates to CRT compared with patients with ischemic cardiomyopathy...
February 2016: Journal of Atrial Fibrillation
https://www.readbyqxmd.com/read/27908971/13n-ammonia-pet-ct-detection-of-myocardial-perfusion-abnormalities-in-beagle-dogs-after-local-heart-irradiation
#14
Jianbo Song, Rui Yan, Zhifang Wu, Jianguo Li, Min Yan, Xinzhong Hao, Jianzhong Liu, Sijin Li
: To determine the potential value of (13)N-ammonia positron emission tomography (PET)/computed tomography (CT) myocardial perfusion imaging (MPI) for detection of myocardial perfusion changes at early stage induced by radiation damage. METHODS: Thirty-six Beagle dogs were randomly divided into the control (n = 18) or the irradiation groups (n = 18). The irradiation group underwent local irradiation to the left ventricular anterior cardiac wall with a single dose of 20 Gy, whereas the control group received sham irradiation...
December 1, 2016: Journal of Nuclear Medicine: Official Publication, Society of Nuclear Medicine
https://www.readbyqxmd.com/read/27906521/modeling-the-human-scarred-heart-in-vitro-toward-new-tissue-engineered-models
#15
Janine C Deddens, Amir Hossein Sadeghi, Jesper Hjortnaes, Linda W van Laake, Marc Buijsrogge, Pieter A Doevendans, Ali Khademhosseini, Joost P G Sluijter
Cardiac remodeling is critical for effective tissue healing, however, excessive production and deposition of extracellular matrix components contribute to scarring and failing of the heart. Despite the fact that novel therapies have emerged, there are still no lifelong solutions for this problem. An urgent need exists to improve the understanding of adverse cardiac remodeling in order to develop new therapeutic interventions that will prevent, reverse, or regenerate the fibrotic changes in the failing heart...
December 1, 2016: Advanced Healthcare Materials
https://www.readbyqxmd.com/read/27906101/characterization-of-a-dmd-egfp-reporter-mouse-as-a-tool-to-investigate-dystrophin-expression
#16
Mina V Petkova, Susanne Morales-Gonzales, Karima Relizani, Esther Gill, Franziska Seifert, Josefine Radke, Werner Stenzel, Luis Garcia, Helge Amthor, Markus Schuelke
BACKGROUND: Dystrophin is a rod-shaped cytoplasmic protein that provides sarcolemmal stability as a structural link between the cytoskeleton and the extracellular matrix via the dystrophin-associated protein complex (DAPC). Mutations in the dystrophin-encoding DMD gene cause X-linked dystrophinopathies with variable phenotypes, the most severe being Duchenne muscular dystrophy (DMD) characterized by progressive muscle wasting and fibrosis. However, dystrophin deficiency does not only impair the function of skeletal and heart muscle but may also affect other organ systems such as the brain, eye, and gastrointestinal tract...
July 5, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27904843/cardiac-surgery-in-africa-a-thirty-five-year-experience-on-open-heart-surgery-in-cote-d-ivoire
#17
Koffi Herve Yangni-Angate, Christophe Meneas, Florent Diby, Manga Diomande, Anicet Adoubi, Yves Tanauh
BACKGROUND: Few centers for open heart surgery (OHS) are in Sub-Saharan Africa. Lack of OHS results is also noted. By reporting our African experience on OHS, the aim of this study was to fill the gap. METHODS: It is a retrospective study on 2,612 patients who were subject to an OHS between 1978 and 2013. Data were collected from demographical, clinical, investigative studies, surgical and outcomes parameters. RESULTS: There were 1,475 cases of rheumatic heart diseases (RHD), 126 endomyocardial fibrosis (EMF), 741 congenital heart diseases (CHDs) and 270 various affections...
October 2016: Cardiovascular Diagnosis and Therapy
https://www.readbyqxmd.com/read/27904687/high-fructose-causes-cardiac-hypertrophy-via-mitochondrial-signaling-pathway
#18
Yan-Bo Zhang, Yan-Hai Meng, Shuo Chang, Rong-Yuan Zhang, Chen Shi
High fructose diet can cause cardiac hypertrophy and oxidative stress is a key mediator for myocardial hypertrophy. Disruption of cystic fibrosis transmembrane conductance regulator (CFTR) leads to oxidative stress. This study aims to reveal mitochondrial oxidative stress-related signaling pathway in high fructose-induced cardiac hypertrophy. Mice were fed high fructose to develop cardiac hypertrophy. Fructose and H2O2 were used to induce cardiomyocyte hypertrophy in vitro. Mitochondria-targeted antioxidant SkQ1 was applied to investigate the possible role of mitochondrial reactive oxygen species (ROS)...
2016: American Journal of Translational Research
https://www.readbyqxmd.com/read/27904669/astragaloside-iv-enhances-cardioprotection-of-remote-ischemic-conditioning-after-acute-myocardial-infarction-in-rats
#19
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
https://www.readbyqxmd.com/read/27903744/metallothionein-is-downstream-of-nrf2-and-partially-mediates-sulforaphane-prevention-of-diabetic-cardiomyopathy
#20
Junlian Gu, Yanli Cheng, Hao Wu, Lili Kong, Shudong Wang, Zheng Xu, Zhiguo Zhang, Yi Tan, Bradley B Keller, Honglan Zhou, Yuehui Wang, Zhonggao Xu, Lu Cai
We have reported that sulforaphane prevented diabetic cardiomyopathy in both T1DM and T2DM animal models via the up-regulation of Nrf2 and metallothionein (MT). Here we tested whether sulforaphane protects the heart from T2DM directly through Nrf2, MT or both. Using Nrf2-knockout (KO), MT-KO, and wild-type mice T2DM was induced by feeding high-fat diet (HFD) for 3 months followed by a small dose of streptozotocin. Age-matched controls were given normal diet (ND). Both T2DM and control mice were then treated with or without sulforaphane for 4 months with continually feeding HFD or ND...
November 30, 2016: Diabetes
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