| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Roger S Y Foo, Richard C M Siow, Morris J Brown, Martin R Bennet. Heme oxygenase-1 gene transfer inhibits angiotensin II-mediated rat cardiac myocyte apoptosis but not hypertrophy. Journal of cellular physiology. vol 209. issue 1. 2006-10-20. PMID:16826603. |
our findings identify the signalling pathways by which ho-1 gene transfer protects against apoptosis and suggest that overexpression of ho-1 in cardiomyopathies may delay the transition from myocyte hypertrophy to heart failure. |
2006-10-20 |
2023-08-12 |
rat |
| Laura A DiMichele, Jason T Doherty, Mauricio Rojas, Hilary E Beggs, Louis F Reichardt, Christopher P Mack, Joan M Taylo. Myocyte-restricted focal adhesion kinase deletion attenuates pressure overload-induced hypertrophy. Circulation research. vol 99. issue 6. 2006-10-12. PMID:16902179. |
these studies show that loss of fak impairs normal compensatory hypertrophic remodeling without a concomitant increase in apoptosis in response to cardiac pressure overload and highlight the possibility that fak activation may be a common requirement for the initiation of this compensatory response. |
2006-10-12 |
2023-08-12 |
mouse |
| Marzia Lotrionte, Leda Galiuto, Giuseppe G L Biondi-Zoccai, Antonio Abbat. [Pathophysiologic role of myocardial hypertrophy, microcirculatory dysfunction and cardiomyocyte apoptosis in aortic stenosis]. Giornale italiano di cardiologia (2006). vol 7. issue 7. 2006-10-12. PMID:16977783. |
[pathophysiologic role of myocardial hypertrophy, microcirculatory dysfunction and cardiomyocyte apoptosis in aortic stenosis]. |
2006-10-12 |
2023-08-12 |
Not clear |
| Marzia Lotrionte, Leda Galiuto, Giuseppe G L Biondi-Zoccai, Antonio Abbat. [Pathophysiologic role of myocardial hypertrophy, microcirculatory dysfunction and cardiomyocyte apoptosis in aortic stenosis]. Giornale italiano di cardiologia (2006). vol 7. issue 7. 2006-10-12. PMID:16977783. |
most recently, experimental studies in animals and clinical studies in humans have shown that myocardial hypertrophy, microcirculatory dysfunction and cardiomyocyte apoptosis are among the central pathophysiologic mechanisms involved in the natural history of aortic stenosis, i.e. |
2006-10-12 |
2023-08-12 |
Not clear |
| Koji Kusaka, Hiroshi Imamura, Tomoaki Tomiya, Tadatoshi Takayama, Masatoshi Makuuch. Expression of transforming growth factor-alpha and -beta in hepatic lobes after hemihepatic portal vein embolization. Digestive diseases and sciences. vol 51. issue 8. 2006-10-10. PMID:16838117. |
in conclusion, these findings indicate that tgf-alpha and tgf-beta expression (assessed by immunohistochemical staining) increase in relation to hepatocyte proliferation and apoptosis, respectively, after pve in humans and the balance of the two factors may contribute to hepatic atrophy and hypertrophy concomitantly observed in this model. |
2006-10-10 |
2023-08-12 |
Not clear |
| Yanling Zhang, Jun Wada, Izumi Hashimoto, Jun Eguchi, Akihiro Yasuhara, Yashpal S Kanwar, Kenichi Shikata, Hirofumi Makin. Therapeutic approach for diabetic nephropathy using gene delivery of translocase of inner mitochondrial membrane 44 by reducing mitochondrial superoxide production. Journal of the American Society of Nephrology : JASN. vol 17. issue 4. 2006-09-28. PMID:16510762. |
the gene delivery alleviated proteinuria and renal hypertrophy at 8 wk after the injection, inhibited renal cell proliferation and apoptosis, and suppressed superoxide production. |
2006-09-28 |
2023-08-12 |
mouse |
| E L Lushnikova, L M Nepomniashchik. [Genetic factors of the development of dilated cardiomyopathy]. Vestnik Rossiiskoi akademii meditsinskikh nauk. issue 7. 2006-09-26. PMID:16924878. |
cardiomyocyte apoptosis can be intensified as a result of changes in signaling transduction (modifications of the expression of some receptors), ionic homeostasis, intensity of metabolic reactions, and due to cardiomyocyte compensatory hypertrophy, which is characterized by expression of some embryonic genes. |
2006-09-26 |
2023-08-12 |
Not clear |
| Renate B Pilz, Kate E Broderic. Role of cyclic GMP in gene regulation. Frontiers in bioscience : a journal and virtual library. vol 10. 2006-09-18. PMID:15769622. |
cyclic gmp is produced in response to nitric oxide and natriuretic peptides; cgmp is a key regulator of cell proliferation, differentiation, and apoptosis, and plays an important role in many (patho)physiological processes such as synaptic plasticity, angiogenesis, inflammation, and cardiac hypertrophy. |
2006-09-18 |
2023-08-12 |
mouse |
| Hiroyuki Tsutsu. Mitochondrial oxidative stress and heart failure. Internal medicine (Tokyo, Japan). vol 45. issue 13. 2006-09-15. PMID:16880705. |
reactive oxygen species induce myocyte hypertrophy, apoptosis, and interstitial fibrosis by activating matrix metalloproteinases. |
2006-09-15 |
2023-08-12 |
Not clear |
| Shin-Da Lee, Chun-Hsien Chu, Erh-Jung Huang, Min-Chi Lu, Jer-Yuh Liu, Chung-Jung Liu, Hsi-Hsien Hsu, James A Lin, Wei-Wen Kuo, Chih-Yang Huan. Roles of insulin-like growth factor II in cardiomyoblast apoptosis and in hypertensive rat heart with abdominal aorta ligation. American journal of physiology. Endocrinology and metabolism. vol 291. issue 2. 2006-09-12. PMID:16825605. |
although igf-ii activating the igf-ii receptor signaling pathway has been found to stimulate cardiomyocyte hypertrophy, the role of igf-ii in cardiac cell apoptosis remains unclear. |
2006-09-12 |
2023-08-12 |
rat |
| Young I Lee, Joon Y Cho, Mun H Kim, Kee B Kim, Dong J Lee, Kyu S Le. Effects of exercise training on pathological cardiac hypertrophy related gene expression and apoptosis. European journal of applied physiology. vol 97. issue 2. 2006-08-29. PMID:16583233. |
effects of exercise training on pathological cardiac hypertrophy related gene expression and apoptosis. |
2006-08-29 |
2023-08-12 |
rat |
| Young I Lee, Joon Y Cho, Mun H Kim, Kee B Kim, Dong J Lee, Kyu S Le. Effects of exercise training on pathological cardiac hypertrophy related gene expression and apoptosis. European journal of applied physiology. vol 97. issue 2. 2006-08-29. PMID:16583233. |
these findings suggest that exercise training prevents pathological hypertrophy in the left ventricle by modulation of myocardial genes and that it interferes with a signal transduction pathway of apoptosis secondary to the pathological cardiac hypertrophy. |
2006-08-29 |
2023-08-12 |
rat |
| Xinli Zhang, Catherine M Cowan, Xinquan Jiang, Chia Soo, Steve Miao, Dale Carpenter, Benjamin Wu, Shun'ichi Kuroda, Kang Tin. Nell-1 induces acrania-like cranioskeletal deformities during mouse embryonic development. Laboratory investigation; a journal of technical methods and pathology. vol 86. issue 7. 2006-08-23. PMID:16652108. |
in addition, transgenic e15.5 and newborn transgenic mice with the cs phenotype displayed distortion of the chondrocranium associated with premature hypertrophy and increased apoptosis of chondrocytes. |
2006-08-23 |
2023-08-12 |
mouse |
| Julie Chao, Grant Bledsoe, Hang Yin, Lee Cha. The tissue kallikrein-kinin system protects against cardiovascular and renal diseases and ischemic stroke independently of blood pressure reduction. Biological chemistry. vol 387. issue 6. 2006-08-22. PMID:16800727. |
kallikrein has pleiotropic effects in inhibiting apoptosis, inflammation, proliferation, hypertrophy and fibrosis, and promoting angiogenesis and neurogenesis in different experimental animal models. |
2006-08-22 |
2023-08-12 |
mouse |
| Michelle T Barati, Madhavi J Rane, Jon B Klein, Kenneth R McLeis. A proteomic screen identified stress-induced chaperone proteins as targets of Akt phosphorylation in mesangial cells. Journal of proteome research. vol 5. issue 7. 2006-08-22. PMID:16823971. |
the serine-threonine kinase akt regulates mesangial cell apoptosis, proliferation, and hypertrophy. |
2006-08-22 |
2023-08-12 |
rat |
| P Tsibiribi, C Bui-Xuan, B Bui-Xuan, C Lombard-Bohas, S Duperret, M Belkhiria, A Tabib, G Maujean, J Descotes, Q Timou. Cardiac lesions induced by 5-fluorouracil in the rabbit. Human & experimental toxicology. vol 25. issue 6. 2006-08-22. PMID:16866187. |
repeated infusions of 15 mg/kg 5fu induced left ventricular hypertrophy, foci of myocardial necrosis, thickening of intra-myocardial arterioles, and disseminated apoptosis in myocardial cells of the epicardium, as well as endothelial cells of the distal coronary arteries. |
2006-08-22 |
2023-08-12 |
rabbit |
| Ieng-Yi Chen, Jacqueline Lypowy, Jayashree Pain, Danish Sayed, Stan Grinberg, Ralph R Alcendor, Junichi Sadoshima, Maha Abdellati. Histone H2A.z is essential for cardiac myocyte hypertrophy but opposed by silent information regulator 2alpha. The Journal of biological chemistry. vol 281. issue 28. 2006-08-21. PMID:16687393. |
an increase in sir2alpha also resulted in a dose-dependent reduction of the response to hypertrophic stimuli, whereas its inhibition resulted in enhanced hypertrophy and apoptosis. |
2006-08-21 |
2023-08-12 |
Not clear |
| Ieng-Yi Chen, Jacqueline Lypowy, Jayashree Pain, Danish Sayed, Stan Grinberg, Ralph R Alcendor, Junichi Sadoshima, Maha Abdellati. Histone H2A.z is essential for cardiac myocyte hypertrophy but opposed by silent information regulator 2alpha. The Journal of biological chemistry. vol 281. issue 28. 2006-08-21. PMID:16687393. |
in short, the results suggest that h2a.z is required for cardiac hypertrophy, where its stability and the extent of cell growth and apoptosis are moderated by sir2alpha. |
2006-08-21 |
2023-08-12 |
Not clear |
| Katrien Lemmens, Vincent F M Segers, Marc Demolder, Gilles W De Keulenae. Role of neuregulin-1/ErbB2 signaling in endothelium-cardiomyocyte cross-talk. The Journal of biological chemistry. vol 281. issue 28. 2006-08-21. PMID:16698793. |
pretreating cardiomyocytes with these inhibitory anti-erbb2 antibodies significantly attenuated cmve-induced cardiomyocyte hypertrophy and abolished the protective actions of cmve against cardiomyocyte apoptosis. |
2006-08-21 |
2023-08-12 |
rat |
| Susanne Rutschow, Jun Li, Heinz-Peter Schultheiss, Matthias Pauschinge. Myocardial proteases and matrix remodeling in inflammatory heart disease. Cardiovascular research. vol 69. issue 3. 2006-08-18. PMID:16417902. |
the myocardial inflammatory reaction not only affects myocardial hypertrophy and apoptosis, but it has a major influence on the regulation of extracellular matrix turnover. |
2006-08-18 |
2023-08-12 |
Not clear |