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Angiogenesis cardiac failure

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https://www.readbyqxmd.com/read/29777508/endothelial-progenitor-cells-in-heart-failure-an-authentic-expectation-for-potential-future-use-and-a-lack-of-universal-definition
#1
REVIEW
Andie H Djohan, Ching-Hui Sia, Poay Sian Lee, Kian-Keong Poh
Congestive heart failure (CHF) is a prevalent disease (especially among the elderly) with high mortality and morbidity rates. The pathological hallmark of CHF is a loss of cardiomyocytes leading to cardiac fibrosis and dysfunctional cardiac remodeling, which culminates in organ failure. Endothelial progenitor cells (EPCs) are bone marrow-derived cells that contribute to maintenance of the integrity of endothelial wall and protect ischemic myocardium through forming new blood vessels (vasculogenesis) or proliferation of pre-existing vasculature (angiogenesis)...
May 17, 2018: Journal of Cardiovascular Translational Research
https://www.readbyqxmd.com/read/29752300/intramyocardial-angiogenetic-stem-cells-and-epicardial-erythropoietin-save-the-acute-ischemic-heart
#2
Christian Klopsch, Anna Skorska, Marion Ludwig, Heiko Lemcke, Gabriela Maass, Ralf Gaebel, Martin Beyer, Cornelia Lux, Anita Toelk, Karina Müller, Christian Maschmeier, Sarah Rohde, Petra Mela, Brigitte Müller-Hilke, Stefan Jockenhoevel, Brigitte Vollmar, Robert Jaster, Robert David, Gustav Steinhoff
Ischemic heart failure still displays the highest mortality. An early boost of intracardiac regenerative key mechanisms and angiogenetic niche signaling in cardiac mesenchymal stem cells (MSCs) could improve myocardial infarction (MI) healing. Epicardial erythropoietin (EPO, 300U kg-1 ) was compared with intraperitoneal and intramyocardial EPO treatments after acute MI in rats (n=156). Real-time PCR and confocal microscopy revealed epicardial EPO treatment enhanced intracardiac regenerative key indicators (SDF-1, CXCR-4, CD34, Bcl-2, Cyclin D1, Cdc2, MMP2), induced TGF-β/WNT signaling in intramyocardial MSC niches through direct activation of AKT, upregulations of upstream signals FOS and Fzd7 and augmented intracardiac mesenchymal proliferation 24 hours after MI...
May 10, 2018: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/29732375/vascular-endothelial-growth-factor-b-and-its-signaling
#3
Nathaniel Lal, Karanjit Puri, Brian Rodrigues
In diabetes, compromised glucose utilization leads the heart to use FA almost exclusively for ATP generation. Chronically, this adaptation unfortunately leads to the conversion of FA to potentially toxic FA metabolites. Paired with increased formation of reactive oxygen species related to excessive mitochondrial oxidation of FA, can provoke cardiac cell death. To protect against this cell demise, intrinsic mechanisms must be available to the heart. Vascular endothelial growth factor B (VEGFB) may be one growth factor that plays an important role in protecting against heart failure...
2018: Frontiers in Cardiovascular Medicine
https://www.readbyqxmd.com/read/29712858/distinct-roles-of-resident-and-nonresident-macrophages-in-nonischemic-cardiomyopathy
#4
Xudong Liao, Yuyan Shen, Rongli Zhang, Keiki Sugi, Neelakantan T Vasudevan, M Amer Alaiti, David R Sweet, Lin Zhou, Yulan Qing, Stanton L Gerson, Chen Fu, Anthony Wynshaw-Boris, Rui Hu, Martin A Schwartz, Hisashi Fujioka, Brian Richardson, Mark J Cameron, Hiroki Hayashi, Jonathan S Stamler, Mukesh K Jain
Nonischemic cardiomyopathy (NICM) resulting from long-standing hypertension, valvular disease, and genetic mutations is a major cause of heart failure worldwide. Recent observations suggest that myeloid cells can impact cardiac function, but the role of tissue-intrinsic vs. tissue-extrinsic myeloid cells in NICM remains poorly understood. Here, we show that cardiac resident macrophage proliferation occurs within the first week following pressure overload hypertrophy (POH; a model of heart failure) and is requisite for the heart's adaptive response...
April 30, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29703647/adeno-associated-virus-gene-therapy-translational-progress-and-future-prospects-in-the-treatment-of-heart-failure
#5
REVIEW
Sebastian Bass-Stringer, Bianca C Bernardo, Clive N May, Colleen J Thomas, Kate L Weeks, Julie R McMullen
Despite advances in treatment over the past decade, heart failure remains a significant public health burden and a leading cause of death in the developed world. Gene therapy provides a promising approach for preventing and reversing cardiac abnormalities, however, clinical application has shown limited success to date. A substantial effort is being invested into the development of recombinant adeno-associated viruses (AAVs) for cardiac gene therapy as AAV gene therapy offers a high safety profile and provides sustained and efficient transgene expression following a once-off administration...
March 17, 2018: Heart, Lung & Circulation
https://www.readbyqxmd.com/read/29689347/regulation-of-cardiovascular-development-and-homeostasis-by-the-adrenomedullin-ramp-system
#6
Takayuki Shindo, Megumu Tanaka, Akiko Kamiyoshi, Yuka Ichikawa-Shindo, Hisaka Kawate, Akihiro Yamauchi, Takayuki Sakurai
Adrenomedullin (AM), a member of the calcitonin peptide superfamily, is a peptide involved in both the pathogenesis of cardiovascular diseases and circulatory homeostasis. Its receptor, calcitonin receptor-like receptor (CLR), associates with an accessory protein, receptor activity-modifying protein (RAMP). Depending upon which the three RAMP isoforms (RAMP1-3) it interacts with, CLR functions as a receptor for AM or other calcitonin family peptides. AM knockout mice (-/-) died mid-gestation due to abnormalities in vascular development...
April 21, 2018: Peptides
https://www.readbyqxmd.com/read/29668847/adiponectin-determines-farnesoid-x-receptor-agonism-mediated-cardioprotection-against-post-infarction-remodeling-and-dysfunction
#7
Yunlong Xia, Fuyang Zhang, Shihao Zhao, Yueyang Li, Xiyao Chen, Erhe Gao, Xinyue Xu, Zhenyu Xiong, Xiaomeng Zhang, Jinglong Zhang, Huishou Zhao, Wei Wang, Helin Wang, Yanjie Guo, Yi Liu, Congye Li, Shan Wang, Ling Zhang, Wenjun Yan, Ling Tao
Aims: The farnesoid X receptor (FXR) is a member of the metabolic nuclear receptor superfamily that plays a critical regulatory role in cardiovascular physiology/pathology. However, the role of systemic FXR activation in the chronic phase in myocardial infarction (MI)-induced cardiac remodeling and dysfunction remains unclear. In this study, we aimed to elucidate the role of long-term FXR activation on post-MI cardiac remodeling and dysfunction. Methods and Results: Mice underwent either MI surgery or sham operation...
April 14, 2018: Cardiovascular Research
https://www.readbyqxmd.com/read/29666587/cardioprotective-effects-of-qishenyiqi-dripping-pills-on-transverse-aortic-constriction-induced-heart-failure-in-mice
#8
Guoran Ruan, Haojin Ren, Chi Zhang, Xiaogang Zhu, Chao Xu, Liyue Wang
QiShenYiQi dripping pills (QSYQ), a traditional Chinese medicine, are commonly used to treat coronary heart disease, and QSYQ was recently approved as a complementary treatment for ischemic heart failure in China. However, only few studies reported on whether QSYQ exerts a protective effect on heart failure induced by pressure overload. In this study, we explored the role of QSYQ in a mouse model of heart failure induced by transverse aortic constriction (TAC). Twenty-eight C57BL/6J mice were divided into four groups: Sham + NS group, Sham + QSYQ group, TAC + NS group, and TAC + QSYQ group...
2018: Frontiers in Physiology
https://www.readbyqxmd.com/read/29658862/progress-in-gene-therapy-for-chronic-heart-failure
#9
Zhi-Qiang Yin, Wan-Hong Xing
Chronic heart failure (CHF) is still the leading cause of morbidity and mortality worldwide, and carries with it large economic and social burdens. Although steady and substantial progress has been made in reducing mortality from heart failure using conventional treatments, novel pharmacologic and surgical interventions have not been effective in extending five year survival rates. Therefore, it is necessary to explore new therapies. Gene therapy was introduced in 1970s with the development of recombinant DNA technology...
March 5, 2018: Heart Surgery Forum
https://www.readbyqxmd.com/read/29626503/hsf1-deficiency-accelerates-the-transition-from-pressure-overload-induced-cardiac-hypertrophy-to-heart-failure-through-endothelial-mir-195a-3p-mediated-impairment-of-cardiac-angiogenesis
#10
Shijun Wang, Jian Wu, Jieyun You, Hongyu Shi, Xiaoyu Xue, Jiayuan Huang, Lei Xu, Guoliang Jiang, Lingyan Yuan, Xue Gong, Haiyan Luo, Junbo Ge, Zhaoqiang Cui, Yunzeng Zou
Heat shock transcription factor 1 (HSF1) deficiency aggravates cardiac remodeling under pressure overload. However, the mechanism is still unknown. Here we employed microRNA array analysis of the heart tissue of HSF1-knockout (KO) mice to investigate the potential roles of microRNAs in pressure overload-induced cardiac remodeling under HSF-1 deficiency, and the profiles of 478 microRNAs expressed in the heart tissues of adult HSF1-KO mice were determined. We found that the expression of 5 microRNAs was over 2-fold higher expressed in heart tissues of HSF1-KO mice than in those of wild-type (WT) control mice...
April 4, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29581851/mir-124-aggravates-failing-hearts-by-suppressing-cd151-facilitated-angiogenesis-in-heart
#11
Yanru Zhao, Mengwen Yan, Chen Chen, Wei Gong, Zhongwei Yin, Huaping Li, Jiahui Fan, Xin A Zhang, Dao Wen Wang, Houjuan Zuo
Heart failure (HF) is the final common pathway of various cardiovascular diseases. Although it is well documented that reduction of cardiac angiogenesis contributes to the progression from adaptive cardiac hypertrophy to HF, the molecular mechanisms remain unknown. In the present study, we found that cardiac expression of miR-124 was increased in patients and mice with HF. Recombinant adeno-associated virus (rAAV)-mediated miR-124 over-expression aggravated angiotensin II (Ang II) infusion-induced cardiac dysfunction and abnormal cardiac angiogenesis in mice...
March 6, 2018: Oncotarget
https://www.readbyqxmd.com/read/29577955/adrenomedullin-continuing-to-explore-cardioprotection
#12
Toshihiro Tsuruda, Johji Kato, Kenji Kuwasako, Kazuo Kitamura
Adrenomedullin (AM), a peptide isolated from an extract of human pheochromocytoma, comprises 52 amino acids with an intramolecular disulfide bond and amidation at the carboxy-terminus. AM is present in various tissues and organs in rodents and humans, including the heart. The peptide concentration increases with cardiac hypertrophy, acute myocardial infarction, and overt heart failure in the plasma and the myocardium. The principal function of AM in the cardiovascular system is the regulation of the vascular tone by vasodilation and natriuresis via cyclic adenosine monophosphate-dependent or -independent mechanism...
March 22, 2018: Peptides
https://www.readbyqxmd.com/read/29569957/protein-tyrosine-phosphatase-1b-inactivation-limits-aging-associated-heart-failure-in-mice
#13
Marie Besnier, David Coquerel, Julie Favre, Anais Dumesnil, Dominique Guerrot, Isabelle Remy-Jouet, Paul Mulder, Zoubir Djerada, Fabienne Tamion, Vincent Richard, Antoine Ouvrard-Pascaud
Background- We previously showed that Protein Tyrosine Phosphatase 1B inactivation (PTP1B-/- ) in mice improved left ventricular (LV) angiogenesis, perfusion, remodeling and function, and limits endothelial dysfunction after myocardial infarction. However, whether PTP1B inactivation slows aging-associated cardiovascular dysfunction remains unknown. Methods and Results- WT and PTP1B-/- mice were allowed to age until 18 months. Compared to old WT in which aging increased the LV mRNA expression of PTP1B, old PTP1B-/- mice had: 1) reduced cardiac hypertrophy with decreased LV mRNA levels of hypertrophic markers, atrial and brain natriuretic peptides; 2) lower LV fibrosis (collagen: WT 16{plus minus}3, PTP1B-/- 5{plus minus}3 %, p<0...
March 23, 2018: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29534229/ceramide-1-phosphate-has-protective-properties-against-cyclophosphamide-induced-ovarian-damage-in-a-mice-model-of-premature-ovarian-failure
#14
Natalia Pascuali, Leopoldina Scotti, Mariana Di Pietro, Gonzalo Oubiña, Diana Bas, María May, Antonio Gómez Muñoz, Patricia S Cuasnicú, Débora J Cohen, Marta Tesone, Dalhia Abramovich, Fernanda Parborell
STUDY QUESTION: Is ceramide-1-phosphate (C1P) an ovarian protective agent during alkylating chemotherapy? SUMMARY ANSWER: Local administration of C1P drastically reduces ovarian damage induced by cyclophosphamide (Cy) via protection of follicular reserve, restoration of hormone levels, inhibition of apoptosis and improvement of stromal vasculature, while protecting fertility, oocyte quality and uterine morphology. WHAT IS KNOWN ALREADY: Cancer-directed therapies cause accelerated loss of ovarian reserve and lead to premature ovarian failure (POF)...
May 1, 2018: Human Reproduction
https://www.readbyqxmd.com/read/29508011/imaging-with-ultrasound-contrast-agents-current-status-and-future
#15
REVIEW
Wui K Chong, Virginie Papadopoulou, Paul A Dayton
Microbubble ultrasound contrast agents (UCAs) were recently approved by the Food and Drug administration for non-cardiac imaging. The physical principles of UCAs, methods of administration, dosage, adverse effects, and imaging techniques both current and future are described. UCAs consist of microbubbles in suspension which strongly interact with the ultrasound beam and are readily detectable by ultrasound imaging systems. They are confined to the blood pool when administered intravenously, unlike iodinated and gadolinium contrast agents...
April 2018: Abdominal Radiology
https://www.readbyqxmd.com/read/29507857/importance-of-physical-capacity-and-the-effects-of-exercise-in-heart-transplant-recipients
#16
REVIEW
Marianne Yardley, Lars Gullestad, Kari Nytrøen
One of the most important prognostic factors in heart failure patients is physical capacity. Patients with very poor physical performance and otherwise eligible, may be listed as candidates for heart transplantation (HTx). After such surgery, life-long immunosuppression therapy is needed to prevent rejection of the new heart. The dark side of immunosuppression is the increased risk of infections, kidney failure, cancer and advanced atherosclerosis (cardiac allograft vasculopathy), with the two latter conditions as the main causes of later mortality...
February 24, 2018: World Journal of Transplantation
https://www.readbyqxmd.com/read/29353241/inhibition-of-endothelial-notch-signaling-impairs-fatty-acid-transport-and-leads-to-metabolic-and-vascular-remodeling-of-the-adult-heart
#17
Markus Jabs, Adam J Rose, Lorenz H Lehmann, Jacqueline Taylor, Iris Moll, Tjeerd P Sijmonsma, Stefanie E Herberich, Sven W Sauer, Gernot Poschet, Giuseppina Federico, Carolin Mogler, Eva-Maria Weis, Hellmut G Augustin, Minhong Yan, Norbert Gretz, Roland M Schmid, Ralf H Adams, Hermann-Joseph Gröne, Rüdiger Hell, Jürgen G Okun, Johannes Backs, Peter P Nawroth, Stephan Herzig, Andreas Fischer
Background -Nutrients are transported through endothelial cells before being metabolized in muscle cells. However, little is known about the regulation of endothelial transport processes. Notch signaling is a critical regulator of metabolism and angiogenesis during development. Here, we studied how genetic and pharmacological manipulation of endothelial Notch signaling in adult mice affects endothelial fatty acid transport, cardiac angiogenesis, and heart function. Methods -Endothelial-specific Notch inhibition was achieved by conditional genetic inactivation of Rbp-jκ in adult mice to analyze fatty acid metabolism and heart function...
January 20, 2018: Circulation
https://www.readbyqxmd.com/read/29344827/molecular-imaging-of-cardiac-remodelling-after-myocardial-infarction
#18
REVIEW
Daniel Curley, Begoña Lavin Plaza, Ajay M Shah, René M Botnar
Myocardial infarction and subsequent heart failure is a major health burden associated with significant mortality and morbidity in western societies. The ability of cardiac tissue to recover after myocardial infarction is affected by numerous complex cellular and molecular pathways. Unbalance or failure of these pathways can lead to adverse remodelling of the heart and poor prognosis. Current clinical cardiac imaging modalities assess anatomy, perfusion, function, and viability of the myocardium, yet do not offer any insight into the specific molecular pathways involved in the repair process...
January 17, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29259712/pathophysiology-and-therapeutic-potential-of-cardiac-fibrosis
#19
REVIEW
Hironori Hara, Norifumi Takeda, Issei Komuro
Inflammatory and fibrotic responses to myocardial damage are essential for cardiac repair; however, these responses often result in extensive fibrotic remodeling with impaired systolic function. Recent reports have suggested that such acute phase responses provide a favorable environment for endogenous cardiac regeneration, which is mainly driven by the division of pre-existing cardiomyocytes (CMs). Existing CMs in mammals can re-acquire proliferative activity after substantial cardiac damage, and elements other than CMs in the physiological and/or pathological environment, such as hypoxia, angiogenesis, and the polarity of infiltrating macrophages, have been reported to regulate replication...
2017: Inflammation and Regeneration
https://www.readbyqxmd.com/read/29249393/therapeutic-benefit-and-gene-network-regulation-by-combined-gene-transfer-of-apelin-fgf2-and-serca2a-into-ischemic-heart
#20
Edith Renaud-Gabardos, Florence Tatin, Fransky Hantelys, Benoît Lebas, Denis Calise, Oksana Kunduzova, Bernard Masri, Françoise Pujol, Pierre Sicard, Philippe Valet, Jérôme Roncalli, Xavier Chaufour, Barbara Garmy-Susini, Angelo Parini, Anne-Catherine Prats
Despite considerable advances in cardiovascular disease treatment, heart failure remains a public health challenge. In this context, gene therapy appears as an attractive approach, but clinical trials using single therapeutic molecules result in moderate benefit. With the objective of improving ischemic heart failure therapy, we designed a combined treatment, aimed to simultaneously stimulate angiogenesis, prevent cardiac remodeling, and restore contractile function. We have previously validated IRES-based vectors as powerful tools to co-express genes of interest...
March 7, 2018: Molecular Therapy: the Journal of the American Society of Gene Therapy
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