| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Pål Aukrust, Lars Gullestad, Thor Ueland, Jan K Damås, Arne Yndesta. Inflammatory and anti-inflammatory cytokines in chronic heart failure: potential therapeutic implications. Annals of medicine. vol 37. issue 2. 2005-08-11. PMID:16026115. |
persistent inflammation, involving increased levels of inflammatory cytokines, seems to play a pathogenic role in chronic heart failure (hf) by influencing heart contractility, inducing hypertrophy and promoting apoptosis, contributing to myocardial remodeling. |
2005-08-11 |
2023-08-12 |
Not clear |
| Kan Zen, Hidekazu Irie, Tomoki Doue, Michitaka Takamiya, Tetsuhiro Yamano, Takahisa Sawada, Akihiro Azuma, Hiroaki Matsubar. Analysis of circulating apoptosis mediators and proinflammatory cytokines in patients with idiopathic hypertrophic cardiomyopathy: comparison between nonobstructive and dilated-phase hypertrophic cardiomyopathy. International heart journal. vol 46. issue 2. 2005-08-05. PMID:15876807. |
analysis of circulating apoptosis mediators and proinflammatory cytokines in patients with idiopathic hypertrophic cardiomyopathy: comparison between nonobstructive and dilated-phase hypertrophic cardiomyopathy. |
2005-08-05 |
2023-08-12 |
human |
| C Fiorillo, C Nediani, V Ponziani, L Giannini, A Celli, N Nassi, L Formigli, A M Perna, P Nass. Cardiac volume overload rapidly induces oxidative stress-mediated myocyte apoptosis and hypertrophy. Biochimica et biophysica acta. vol 1741. issue 1-2. 2005-07-29. PMID:15894467. |
cardiac volume overload rapidly induces oxidative stress-mediated myocyte apoptosis and hypertrophy. |
2005-07-29 |
2023-08-12 |
Not clear |
| C Fiorillo, C Nediani, V Ponziani, L Giannini, A Celli, N Nassi, L Formigli, A M Perna, P Nass. Cardiac volume overload rapidly induces oxidative stress-mediated myocyte apoptosis and hypertrophy. Biochimica et biophysica acta. vol 1741. issue 1-2. 2005-07-29. PMID:15894467. |
as plausible candidates for a connection between oxidative stress and cardiomyocyte apoptosis or hypertrophy, we explored the behaviour of two mapks, specifically jnk and erk. |
2005-07-29 |
2023-08-12 |
Not clear |
| C Fiorillo, C Nediani, V Ponziani, L Giannini, A Celli, N Nassi, L Formigli, A M Perna, P Nass. Cardiac volume overload rapidly induces oxidative stress-mediated myocyte apoptosis and hypertrophy. Biochimica et biophysica acta. vol 1741. issue 1-2. 2005-07-29. PMID:15894467. |
oxidative stress markers significantly decreased at 96 h of overload, combined with a marked attenuation of apoptosis and the appearance of hypertrophy. |
2005-07-29 |
2023-08-12 |
Not clear |
| Carmelle V Remillard, Jason X-J Yua. ClC-3: more than just a volume-sensitive Cl- channel. British journal of pharmacology. vol 145. issue 1. 2005-07-28. PMID:15723095. |
pulmonary vascular medial hypertrophy due to enhanced pulmonary artery smooth muscle cell (pasmc) proliferation and/or decreased pasmc apoptosis is a primary cause of increased pulmonary vascular resistance and arterial pressure in patients with pulmonary arterial hypertension. |
2005-07-28 |
2023-08-12 |
rat |
| J Craig Hunter, Donna H Korzic. Protein kinase C distribution and translocation in rat myocardium: Methodological considerations. Journal of pharmacological and toxicological methods. vol 51. issue 2. 2005-07-21. PMID:15767206. |
protein kinase c (pkc) is an important modifier of several cardiovascular phenomena, including cardioprotection, apoptosis, and hypertrophy. |
2005-07-21 |
2023-08-12 |
rat |
| L Centurione, C Di Giulio, E Santavenere, M Cacchio, N Sabatini, C Rapino, G Bianchi, M Rapino, D Bosco, A Antonucci, A Catald. Protein kinase C zeta regulation of hypertrophic and apoptotic events occurring during rat neonatal heart development and growth. International journal of immunopathology and pharmacology. vol 18. issue 1. 2005-07-14. PMID:15698510. |
moreover, hypertrophy is accomplished to apoptosis which controls the final number of myocardial cells, deletes vestigial structures, and takes part in remodelling the organ. |
2005-07-14 |
2023-08-12 |
rat |
| Denis Deblois, Bun-Seng Tea, Diane Beaudry, Pavel Hame. Regulation of therapeutic apoptosis: a potential target in controlling hypertensive organ damage. Canadian journal of physiology and pharmacology. vol 83. issue 1. 2005-07-11. PMID:15759048. |
we first reported that, irrespective of the drug class, those drugs that are able to induce regression of cardiovascular hypertrophy are also able to reverse cardiovascular hyperplasia via apoptosis. |
2005-07-11 |
2023-08-12 |
rat |
| Faisal Syed, Amy Odley, Harvey S Hahn, Eric W Brunskill, Roy A Lynch, Yehia Marreez, Atsushi Sanbe, Jeffrey Robbins, Gerald W Dor. Physiological growth synergizes with pathological genes in experimental cardiomyopathy. Circulation research. vol 95. issue 12. 2005-07-06. PMID:15539635. |
unlike normal postnatal cardiac growth, concurrent left ventricular pressure overload hypertrophy did not synergize with nix expression to cause cardiomyopathy or myocardial apoptosis. |
2005-07-06 |
2023-08-12 |
mouse |
| Teruya Nakamura, Kunio Matsumoto, Shinya Mizuno, Yoshiki Sawa, Hikaru Matsuda, Toshikazu Nakamur. Hepatocyte growth factor prevents tissue fibrosis, remodeling, and dysfunction in cardiomyopathic hamster hearts. American journal of physiology. Heart and circulatory physiology. vol 288. issue 5. 2005-05-31. PMID:15840903. |
likewise, hgf suppressed myocardial hypertrophy, apoptosis in cardiomyocytes, and expression of atrial natriuretic polypeptide, a molecular marker of hypertrophy. |
2005-05-31 |
2023-08-12 |
human |
| Ralph R Alcendor, Lorrie A Kirshenbaum, Shin-ichiro Imai, Stephen F Vatner, Junichi Sadoshim. Silent information regulator 2alpha, a longevity factor and class III histone deacetylase, is an essential endogenous apoptosis inhibitor in cardiac myocytes. Circulation research. vol 95. issue 10. 2005-05-27. PMID:15486319. |
these results suggest that endogenous sir2alpha plays an essential role in mediating cell survival, whereas sir2alpha overexpression protects myocytes from apoptosis and causes modest hypertrophy. |
2005-05-27 |
2023-08-12 |
rat |
| R Cuperus, M G Schäppi, N Shah, K J Lindley, P J Milla, V V Smit. Hypertrophic eosinophilic gastroenteropathy is associated with reduced enterocyte apoptosis. Histopathology. vol 46. issue 1. 2005-05-19. PMID:15656889. |
hypertrophic eosinophilic gastroenteropathy is associated with reduced enterocyte apoptosis. |
2005-05-19 |
2023-08-12 |
Not clear |
| Vili K Stoyanova, Evghenii D Ghenev, Ivan B Yanev, Tony K Yanev, Chudomir K Nache. A reproducible model of cardiac hypertrophy in rats. Problems and obstacles we faced. Folia medica. vol 46. issue 3. 2005-05-12. PMID:15819460. |
to develop a reproducible model of significant left ventricular hypertrophy in order to study the role played by the tumor suppressor protein 53 (p53) in the mechanisms of cardiac hypertrophy, the cross-talk with the other factors and the connection between expression and activity of p53, cardiac myocyte apoptosis and heart hypertrophy; to discuss the problems and obstacles we faced. |
2005-05-12 |
2023-08-12 |
rat |
| Tomasz Urbanek, Barbara Skop, Krzysztof Ziaja, Tadeusz Wilczok, Ryszard Wiaderkiewicz, Artur Pałasz, Urszula Mazurek, Ewa Wielgu. Sapheno-femoral junction pathology: molecular mechanism of saphenous vein incompetence. Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis. vol 10. issue 4. 2005-05-05. PMID:15497017. |
apoptosis downregulation, cell cycle inhibition and smooth muscle cell hypertrophy are important factors influencing vein wall disturbances related to sapheno-femoral junction incompetence. |
2005-05-05 |
2023-08-12 |
human |
| Abdoul Kan. [Beta blockers in the treatment of heart failure due to left ventricular systolic dysfunction]. Dakar medical. vol 48. issue 1. 2005-05-03. PMID:15776641. |
it has been shown that this drugs counteract the negative effects of sympathetic stimulation on the myocardium (myocardial hypertrophy, fibrosis and ischemia arythmogenic effect, increase of cardiac loading, apoptosis). |
2005-05-03 |
2023-08-12 |
Not clear |
| Helmut Walter, Georg Lübbe. Potential role of oral thiazolidinedione therapy in preserving beta-cell function in type 2 diabetes mellitus. Drugs. vol 65. issue 1. 2005-04-25. PMID:15610048. |
insulin resistance, the 'traditional' cornerstone defect of type 2 diabetes, leads to an array of adverse effects on beta cells, including hypertrophy, apoptosis and those caused by lipotoxicity and glucotoxicity. |
2005-04-25 |
2023-08-12 |
rat |
| Lubo Zhan. Prenatal hypoxia and cardiac programming. Journal of the Society for Gynecologic Investigation. vol 12. issue 1. 2005-04-19. PMID:15629664. |
among other effects, chronic hypoxia suppresses fetal cardiac function, alters cardiac gene expression, increases myocyte apoptosis, and results in a premature exit of the cell cycle of cardiomyocytes and myocyte hypertrophy. |
2005-04-19 |
2023-08-12 |
Not clear |
| Ling Ye, Yuji Mishina, Di Chen, Haiyang Huang, Sarah L Dallas, Mark R Dallas, Pitchumani Sivakumar, Tetsuo Kunieda, Takeo W Tsutsui, Adele Boskey, Lynda F Bonewald, Jian Q Fen. Dmp1-deficient mice display severe defects in cartilage formation responsible for a chondrodysplasia-like phenotype. The Journal of biological chemistry. vol 280. issue 7. 2005-04-18. PMID:15590631. |
this phenotype appears to be due to increased cell proliferation in the proliferating zone and reduced apoptosis in the hypertrophic zone. |
2005-04-18 |
2023-08-12 |
mouse |
| Rajasekhar Reddy, Georges Chahoud, J L Meht. Modulation of cardiovascular remodeling with statins: fact or fiction? Current vascular pharmacology. vol 3. issue 1. 2005-04-13. PMID:15638784. |
morphologically the key feature of remodeling is myocyte hypertrophy, myocyte loss from necrosis or apoptosis, as well as interstitial cell growth especially fibroblast proliferation leading to myocardial fibrosis. |
2005-04-13 |
2023-08-12 |
Not clear |