Journal of Cardiothoracic-Renal Research最新文献_第5页

Cyclosporine reduction causes decreasing of angiotensin II and transforming growth factor-beta expression in chronic allograft nephropathy 环孢素减少导致血管紧张素II和转化生长因子- β在慢性同种异体移植肾病中的表达降低

Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.11.005

M. Weir, J. Papadimitriou, C. Drachenberg, Hong Song, S. Bartlett, Chiming Wei

引用次数: 1

Oxidative DNA damage and DNA mismatch repair pathway play an important role in failing human myocardium 氧化性DNA损伤和DNA错配修复途径在人心肌衰竭中起重要作用

Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 DOI: 10.1016/j.jccr.2005.11.004

Ruxian Lin, Daqing Gao, Yesong Gu, Pramod Bonde, Torin P. Fitton, Joshua M. Hare, John V. Conte, G. Melville Williams, Chiming Wei

{"title":"Oxidative DNA damage and DNA mismatch repair pathway play an important role in failing human myocardium","authors":"Ruxian Lin, Daqing Gao, Yesong Gu, Pramod Bonde, Torin P. Fitton, Joshua M. Hare, John V. Conte, G. Melville Williams, Chiming Wei","doi":"10.1016/j.jccr.2005.11.004","DOIUrl":"https://doi.org/10.1016/j.jccr.2005.11.004","url":null,"abstract":"<div><h3>Background</h3><p>Heart failure is approaching epidemic proportions. However, DNA damage in the failing myocardium<span> is not directly addressed yet. 8-Oxo-7,8-dihydrodeoxyguanine (8-oxoG) is a stable marker of DNA damage. The human Mut-Y homologue (hMYH) is a DNA mismatching repair enzyme promoting DNA reconstruction. The current study was designed to investigate whether DNA damage and repair as reflected in the levels of 8-oxoG and hMYH play an important role in the failing myocardium.</span></p></div><div><h3>Methods</h3><p>Donor and failing human myocardium were obtained from hearts of patients undergoing cardiac transplantation<span><span><span>. DNA damage was determined by the presence of 8-oxoG. The protein level, activity, and expression of hMYH were determined by Western blot, the DNA gel-retardation </span>binding assay<span> and immunohistochemical staining (IHCS). The levels of apoptosis and apoptosis-related genes such as p53, p21-WAF, and caspase-3 were determined by </span></span>TUNEL assay and IHCS.</span></p></div><div><h3>Results</h3><p>The levels of 8-oxoG indicating DNA damage significantly increased in the myocardium of failing hearts compared with donor subjects. On the other hand, the protein level and activity of the DNA repair enzyme<span>, hMYH, was significantly decreased in CHF patients compared to donor subjects. Furthermore, apoptosis and apoptosis-related genes such as p53, p21-WAF, and caspase-3 were markedly increased in CHF myocardium.</span></p></div><div><h3>Conclusion</h3><p>Ongoing DNA damage is insufficiently repaired in the myocardium of failing hearts. This appears to be a major pathway responsible for myocardial failure in humans.</p></div>","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Pages 41-49"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2005.11.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72285117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

New sniper assignment for a celebrity—role of endothelin-1 in diabetic cardiomyopathy 名人的新狙击任务——内皮素-1在糖尿病心肌病中的作用

Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 DOI: 10.1016/j.jccr.2005.11.006

Jun Ren , Chiming Wei

{"title":"New sniper assignment for a celebrity—role of endothelin-1 in diabetic cardiomyopathy","authors":"Jun Ren , Chiming Wei","doi":"10.1016/j.jccr.2005.11.006","DOIUrl":"https://doi.org/10.1016/j.jccr.2005.11.006","url":null,"abstract":"<div><p>Diabetic cardiomyopathy is a major threat to increased morbidity and mortality in population with diabetes. A number of hypotheses have been postulated for the pathogenesis of diabetic cardiomyopathy including defective polyol pathway, reduced energy production due to decrease in mitochondrial respiration and pyruvate dehydrogenase activity, accumulation of advanced glycation end-product (AGE) and free radical species, activation of protein kinase C (PKC) as well as enhanced hexosamine flux. These culprit machineries may result in impaired intracellular Ca<sup>2+</sup> handling in cardiomyocytes due to compromised contractile and intracellular Ca<sup>2+</sup> regulatory proteins such as myosin, titin, sarco(endo)plasmic reticulum Ca<sup>2+</sup>-ATPase (SERCA), phospholamban and Na<sup>+</sup>–Ca<sup>2+</sup> exchanger. Nevertheless, neither precise pathogenesis of the disease nor effective therapeutic remedy is available for diabetic cardiomyopathy. In this issue of JCRR, Ding et al. demonstrated an established role of endothelin-1 (ET-1) in diabetes-induced cardiomyocyte dysfunction using treatment of dual ET<sub>A</sub>/ET<sub>B</sub> receptor antagonist bosentan. Their results have conclusively consolidated the logic of ET-1 and its membrane receptors as a novel pathophysiological cue for the development of diabetic cardiomyopathy.</p></div>","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Pages 30-32"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2005.11.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72285120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Stem cells and cardiovascular tissue repair: Mechanism, methods, and clinical applications 干细胞与心血管组织修复：机制、方法和临床应用

Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 DOI: 10.1016/j.jccr.2005.12.003

Qi Zhang , Rosalina Madonna , Weifeng Shen , Emerson Perin , Franca S. Angeli , Ferid Murad , Edward Yeh , L. Maximilian Buja , Raffaele De Caterina , James T. Willerson , Yong-Jian Geng

{"title":"Stem cells and cardiovascular tissue repair: Mechanism, methods, and clinical applications","authors":"Qi Zhang , Rosalina Madonna , Weifeng Shen , Emerson Perin , Franca S. Angeli , Ferid Murad , Edward Yeh , L. Maximilian Buja , Raffaele De Caterina , James T. Willerson , Yong-Jian Geng","doi":"10.1016/j.jccr.2005.12.003","DOIUrl":"https://doi.org/10.1016/j.jccr.2005.12.003","url":null,"abstract":"<div><p><span>Cardiac stem cell therapy is emerging as a potential novel treatment for patients with heart disease. Experimental studies and clinical trials have shown that stem cell transplantation can achieve certain degrees of success in enhancing </span>myocardial perfusion, repair or regeneration, leading to improvement of cardiac function. Different types of stem cells including those from embryonic and adult tissues have been tested, and each stem cell type has advantages and disadvantages. The stem cell type(s) most suitable for cardiac cell therapy is hard to define, but such cells are usually characterized by their high potential for survival, growth, and differentiation as well as integration into the host tissue. Selection of proper delivery methods according to lesion size and location is also a critical factor for the success of stem cell therapy. Preliminary data from experimental stem cell research and clinical trials for cardiac stem cell therapy are controversial, yet encouraging.</p></div>","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Pages 3-14"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2005.12.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72277675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 13

Breaking the barrier of chronic allograft nephropathy (CAN)—Transplant's next major challenge 打破慢性同种异体肾病(CAN)的屏障-移植的下一个主要挑战

Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.12.007

E. Kraus

引用次数: 0

DMNQ S-53 induces apoptosis and inhibits the growth of Lewis lung carcinoma cells in vitro and in vivo DMNQ S-53在体外和体内诱导Lewis肺癌细胞凋亡，抑制Lewis肺癌细胞生长

Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.12.004

Jae‐Ho Lee, Eun Ok Lee, Hyo-Jung Lee, K. Kim, K. Ahn, Sung-Joon Lee, Jiyoung Kim, Sung-Hoon Kim

引用次数: 1