| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Mohammad Amin Kerachian, Chantal Séguin, Edward J Harve. Glucocorticoids in osteonecrosis of the femoral head: a new understanding of the mechanisms of action. The Journal of steroid biochemistry and molecular biology. vol 114. issue 3-5. 2009-06-09. PMID:19429441. |
gcs also cause ischemia through increased intraosseous pressure, which subsequently decreases the blood flow to the femoral head by apoptosis of ecs as well as elevating the level of adipogenesis and fat hypertrophy in the bone marrow. |
2009-06-09 |
2023-08-12 |
Not clear |
| Yeong-Hoon Choi, Douglas B Cowan, Adrian M Moran, Steven D Colan, Christof Stamm, Koh Takeuchi, Ingeborg Friehs, Pedro J del Nido, Francis X McGowa. Myocyte apoptosis occurs early during the development of pressure-overload hypertrophy in infant myocardium. The Journal of thoracic and cardiovascular surgery. vol 137. issue 6. 2009-06-09. PMID:19464448. |
myocyte apoptosis occurs early during the development of pressure-overload hypertrophy in infant myocardium. |
2009-06-09 |
2023-08-12 |
Not clear |
| Haiyun Ling, Tong Zhang, Laetitia Pereira, Christopher Kable Means, Hongqiang Cheng, Yusu Gu, Nancy D Dalton, Kirk L Peterson, Ju Chen, Donald Bers, Joan Heller Brown, Joan Heller Brow. Requirement for Ca2+/calmodulin-dependent kinase II in the transition from pressure overload-induced cardiac hypertrophy to heart failure in mice. The Journal of clinical investigation. vol 119. issue 5. 2009-06-08. PMID:19381018. |
strikingly, while ko mice showed preserved hypertrophy after 6-week tac, camkiidelta deficiency significantly ameliorated phenotypic changes associated with the transition to heart failure, such as chamber dilation, ventricular dysfunction, lung edema, cardiac fibrosis, and apoptosis. |
2009-06-08 |
2023-08-12 |
mouse |
| Carolina D Garciarena, Claudia I Caldiz, Enrique L Portiansky, Gladys E Chiappe de Cingolani, Irene L Enni. Chronic NHE-1 blockade induces an antiapoptotic effect in the hypertrophied heart. Journal of applied physiology (Bethesda, Md. : 1985). vol 106. issue 4. 2009-05-29. PMID:19179646. |
in conclusion, we present data demonstrating that chronic nhe-1 inhibition with cariporide decreases both hypertrophy and apoptosis susceptibility in the spontaneously hypertensive rat heart. |
2009-05-29 |
2023-08-12 |
rat |
| Jian Zhong, Jing Chen, Tingbin Cao, Lijuan Wang, Weiguo Zhang, Daoyan Liu, Zhiming Zh. Adenovirus-mediated FKBP12.6 overexpression induces hypertrophy and apoptosis in cultured neonatal cardiomyocytes. Clinical and experimental pharmacology & physiology. vol 36. issue 2. 2009-05-12. PMID:18759859. |
adenovirus-mediated fkbp12.6 overexpression induces hypertrophy and apoptosis in cultured neonatal cardiomyocytes. |
2009-05-12 |
2023-08-12 |
human |
| Zeenat S Hakim, Laura A DiMichele, Mauricio Rojas, Dane Meredith, Christopher P Mack, Joan M Taylo. FAK regulates cardiomyocyte survival following ischemia/reperfusion. Journal of molecular and cellular cardiology. vol 46. issue 2. 2009-05-05. PMID:19028502. |
myocyte apoptosis is central to myocardial dysfunction following ischemia/reperfusion (i/r) and during the transition from hypertrophy to heart failure. |
2009-05-05 |
2023-08-12 |
Not clear |
| Konstantinos Tziomalos, Joshua M Har. Role of xanthine oxidoreductase in cardiac nitroso-redox imbalance. Frontiers in bioscience (Landmark edition). vol 14. 2009-04-07. PMID:19273066. |
within the heart, xor activity stimulates cardiomyocyte hypertrophy, apoptosis, and impairs matrix structure. |
2009-04-07 |
2023-08-12 |
Not clear |
| H William Schnaper, Sara Jandeska, Constance E Runyan, Susan C Hubchak, Rajit K Basu, Jessica F Curley, Ronald D Smith, Tomoko Hayashid. TGF-beta signal transduction in chronic kidney disease. Frontiers in bioscience (Landmark edition). vol 14. 2009-04-07. PMID:19273211. |
transforming growth factor (tgf)-beta is a central stimulus of the events leading to chronic progressive kidney disease, having been implicated in the regulation of cell proliferation, hypertrophy, apoptosis and fibrogenesis. |
2009-04-07 |
2023-08-12 |
Not clear |
| Narayana Anilkumar, Alexander Sirker, Ajay M Sha. Redox sensitive signaling pathways in cardiac remodeling, hypertrophy and failure. Frontiers in bioscience (Landmark edition). vol 14. 2009-04-07. PMID:19273265. |
in particular, the tightly regulated generation of ros by nadph oxidases appears especially important in key signaling events that drive the development of cardiomyocyte hypertrophy, fibrosis, extracellular matrix remodelling and cell apoptosis. |
2009-04-07 |
2023-08-12 |
Not clear |
| Gerald W Dor. Apoptotic and non-apoptotic programmed cardiomyocyte death in ventricular remodelling. Cardiovascular research. vol 81. issue 3. 2009-03-26. PMID:18779231. |
a defining cellular event in the transition from compensated hypertrophy to dilated cardiomyopathy is cardiomyocyte drop-out due to apoptosis, programmed necrosis, and autophagy. |
2009-03-26 |
2023-08-12 |
Not clear |
| Hiroyuki Tsutsui, Shintaro Kinugawa, Shouji Matsushim. Mitochondrial oxidative stress and dysfunction in myocardial remodelling. Cardiovascular research. vol 81. issue 3. 2009-03-26. PMID:18854381. |
reactive oxygen species induce myocyte hypertrophy, apoptosis, and interstitial fibrosis by activating matrix metalloproteinases. |
2009-03-26 |
2023-08-12 |
Not clear |
| Praveen B Gurpur, Jianming Liu, Dean J Burkin, Stephen J Kaufma. Valproic acid activates the PI3K/Akt/mTOR pathway in muscle and ameliorates pathology in a mouse model of Duchenne muscular dystrophy. The American journal of pathology. vol 174. issue 3. 2009-03-23. PMID:19179609. |
valproic acid (vpa) was found to enhance alpha7 integrin levels, induce muscle hypertrophy, and inhibit apoptosis in myotubes by activating the akt/mtor/p70s6k pathway. |
2009-03-23 |
2023-08-12 |
mouse |
| Jeffrey R Erickson, Mark E Anderso. CaMKII and its role in cardiac arrhythmia. Journal of cardiovascular electrophysiology. vol 19. issue 12. 2009-03-16. PMID:18803570. |
activation of camkii has been linked to important downstream physiological processes, including apoptosis, hypertrophy, and arrhythmia in the heart. |
2009-03-16 |
2023-08-12 |
Not clear |
| Kurt D Meyer, Lubo Zhan. Short- and long-term adverse effects of cocaine abuse during pregnancy on the heart development. Therapeutic advances in cardiovascular disease. vol 3. issue 1. 2009-03-05. PMID:19144667. |
in the rat model, fetal cocaine results in apoptosis in the term heart, left ventricular remodeling and myocyte hypertrophy, as well as increased sensitivity to ischemia/reperfusion injury in the adult male offspring. |
2009-03-05 |
2023-08-12 |
human |
| Ying C Lee, Jens Høiriis Nielse. Regulation of beta cell replication. Molecular and cellular endocrinology. vol 297. issue 1-2. 2009-02-25. PMID:18824066. |
beta cell mass, at any given time, is governed by cell differentiation, neogenesis, increased or decreased cell size (cell hypertrophy or atrophy), cell death (apoptosis), and beta cell proliferation. |
2009-02-25 |
2023-08-12 |
mouse |
| Linan Zhang, Zhe Zhang, Huicai Guo, Yongli Wan. Na+/K+-ATPase-mediated signal transduction and Na+/K+-ATPase regulation. Fundamental & clinical pharmacology. vol 22. issue 6. 2009-02-17. PMID:19049666. |
in cardiac myocytes, the resulting downstream events include the induction of some early response proto-oncogenes, activation of transcription factors, activator protein-1, and nuclear factor-kappab, the regulation of a number of cardiac growth-related genes, and the stimulation of protein synthesis and myocyte hypertrophy and apoptosis. |
2009-02-17 |
2023-08-12 |
Not clear |
| Joel Abramowitz, Lutz Birnbaume. Physiology and pathophysiology of canonical transient receptor potential channels. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. vol 23. issue 2. 2009-02-16. PMID:18940894. |
this analysis reveals trpcs as major and unsuspected gates of ca(2+) entry that contribute, depending on context, to activation of transcription factors, apoptosis, vascular contractility, platelet activation, and cardiac hypertrophy, as well as to normal and abnormal cell proliferation. |
2009-02-16 |
2023-08-12 |
Not clear |
| E G Veste. [Arterial hypertension and cardiac arrhythmias]. Deutsche medizinische Wochenschrift (1946). vol 133 Suppl 8. 2009-02-11. PMID:19085803. |
ventricular arrhythmias: different factors--like hypertrophy, fibrosis, ischemia and apoptosis increase the risk of ventricular arrhythmias and sudden arrhythmic death. |
2009-02-11 |
2023-08-12 |
Not clear |
| Mariane Bertagnolli, Paulo C Schenkel, Cristina Campos, Cristiano T Mostarda, Dulce E Casarini, Adriane Belló-Klein, Maria C Irigoyen, Katya Rigatt. Exercise training reduces sympathetic modulation on cardiovascular system and cardiac oxidative stress in spontaneously hypertensive rats. American journal of hypertension. vol 21. issue 11. 2009-01-30. PMID:18787517. |
spontaneously hypertensive rats (shrs) show increased cardiac sympathetic activity, which could stimulate cardiomyocyte hypertrophy, cardiac damage, and apoptosis. |
2009-01-30 |
2023-08-12 |
rat |
| Zo Rakotoniaina, Pascal Guerard, Frédéric Lirussi, Luc Rochette, Monique Dumas, Françoise Goirand, Marc Bardo. Celecoxib but not the combination of celecoxib+atorvastatin prevents the development of monocrotaline-induced pulmonary hypertension in the rat. Naunyn-Schmiedeberg's archives of pharmacology. vol 378. issue 3. 2009-01-16. PMID:18542928. |
these beneficial effects of celecoxib might be, at least partly, explained by its effects on pulmonary artery thickening and pulmonary hypertrophy, even if it did not show any effect on pulmonary artery vasorelaxation and whole lung enos expression or apoptosis. |
2009-01-16 |
2023-08-12 |
rat |