| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| William Durant. Heme oxygenase-1 in growth control and its clinical application to vascular disease. Journal of cellular physiology. vol 195. issue 3. 2003-05-27. PMID:12704646. |
in addition, ho-1 exerts important effects on critical determinants of tissue size, including cell proliferation, apoptosis, and hypertrophy. |
2003-05-27 |
2023-08-12 |
Not clear |
| Shant Der Sarkissian, Eve-Lyne Marchand, David Duguay, Pavel Hamet, Denis deBloi. Reversal of interstitial fibroblast hyperplasia via apoptosis in hypertensive rat heart with valsartan or enalapril. Cardiovascular research. vol 57. issue 3. 2003-04-30. PMID:12618239. |
renin-angiotensin system inhibitors transiently induce apoptosis at the onset of cardiac hypertrophy regression in spontaneously hypertensive rats (shrs). |
2003-04-30 |
2023-08-12 |
rat |
| Yukiyo Ogata, Masafumi Takahashi, Koichi Takeuchi, Shuichi Ueno, Hiroyuki Mano, Shigeo Ookawara, Eiji Kobayashi, Uichi Ikeda, Kazuyuki Shimad. Fluvastatin induces apoptosis in rat neonatal cardiac myocytes: a possible mechanism of statin-attenuated cardiac hypertrophy. Journal of cardiovascular pharmacology. vol 40. issue 6. 2003-04-29. PMID:12451324. |
fluvastatin induces apoptosis in rat neonatal cardiac myocytes: a possible mechanism of statin-attenuated cardiac hypertrophy. |
2003-04-29 |
2023-08-12 |
rat |
| Yukiyo Ogata, Masafumi Takahashi, Koichi Takeuchi, Shuichi Ueno, Hiroyuki Mano, Shigeo Ookawara, Eiji Kobayashi, Uichi Ikeda, Kazuyuki Shimad. Fluvastatin induces apoptosis in rat neonatal cardiac myocytes: a possible mechanism of statin-attenuated cardiac hypertrophy. Journal of cardiovascular pharmacology. vol 40. issue 6. 2003-04-29. PMID:12451324. |
the findings suggest that fluvastatin induces apoptosis in cardiac myocytes via protein prenylation and the subsequent inhibition of rho, and may play a role in the pathogenesis of cardiac hypertrophy and remodeling. |
2003-04-29 |
2023-08-12 |
rat |
| William T Pu, Qing Ma, Seigo Izum. NFAT transcription factors are critical survival factors that inhibit cardiomyocyte apoptosis during phenylephrine stimulation in vitro. Circulation research. vol 92. issue 7. 2003-04-25. PMID:12663489. |
biomechanical stress on the heart results in activation of numerous signaling cascades, leading to cardiomyocyte hypertrophy, apoptosis, and ultimately, heart failure. |
2003-04-25 |
2023-08-12 |
Not clear |
| William T Pu, Qing Ma, Seigo Izum. NFAT transcription factors are critical survival factors that inhibit cardiomyocyte apoptosis during phenylephrine stimulation in vitro. Circulation research. vol 92. issue 7. 2003-04-25. PMID:12663489. |
we found that selective nfat inhibition during phenylephrine stimulation inhibited hypertrophy but resulted in increased cardiomyocyte apoptosis. |
2003-04-25 |
2023-08-12 |
Not clear |
| Arnold M Kat. Pathophysiology of heart failure: identifying targets for pharmacotherapy. The Medical clinics of North America. vol 87. issue 2. 2003-04-18. PMID:12693727. |
new understanding of the ability of neurohumoral mediators, such as norepinephrine and angiotensin ii, to stimulate remodeling, apoptosis, and other deleterious features of the hypertrophic response has opened important areas for research into the causes and therapy of heart failure. |
2003-04-18 |
2023-08-12 |
Not clear |
| L Gullestad, P Aukrus. The cytokine network in heart failure: pathogenetic importance and potential therapeutic targets. Heart failure monitor. vol 2. issue 1. 2003-04-10. PMID:12634893. |
tumor necrosis factor-a and interleukin-6) have the potential to negatively influence heart contractility, induce hypertrophy, and promote apoptosis or fibrosis, thereby contributing to the continuous remodeling process in chf. |
2003-04-10 |
2023-08-12 |
Not clear |
| Fawzia Huq, Federica Del Monte, Roger J Hajja. Modulating signaling pathways in hypertrophy and heart failure by gene transfer. Journal of cardiac failure. vol 8. issue 6 Suppl. 2003-04-08. PMID:12555151. |
this review highlights recent advances made in the field of myocardial gene transfer, with an emphasis on how manipulation of signal transduction pathways by adenoviral gene transfer has been used to elucidate the pathophysiology underlying abnormal cardiac phenotypes that lead to cardiac failure, such as hypertrophy, contractile dysfunction, and apoptosis. |
2003-04-08 |
2023-08-12 |
Not clear |
| Ayako Nakazono, Fumi Takahashi-Yanaga, Masutaka Furue, Toshiyuki Sasagur. [Caspase-3-mediated alpha-smooth muscle actin cleavage during staurosporine-induced myofibroblast apoptosis]. Nihon yakurigaku zasshi. Folia pharmacologica Japonica. vol 120. issue 1. 2003-04-01. PMID:12491792. |
to examine the possibility that staurosporine is applicable for the treatment of abnormal scar formation such as hypertrophic scar and keloid, the cellular process during staurosporine-induced apoptosis was analyzed in myofibroblasts isolated from a rat granulation tissue pouch. |
2003-04-01 |
2023-08-12 |
rat |
| Ze'ev Hochber. Mechanisms of steroid impairment of growth. Hormone research. vol 58 Suppl 1. 2003-03-17. PMID:12373012. |
direct effects at the growth plate include the suppression of multiple gene expression, chondrocyte proliferation and matrix proteoglycan synthesis, sulfation, release and mineralization as well as the augmentation of hypertrophic cell apoptosis. |
2003-03-17 |
2023-08-12 |
Not clear |
| T Siebler, S M Shalet, H Robso. Effects of chemotherapy on bone metabolism and skeletal growth. Hormone research. vol 58 Suppl 1. 2003-03-17. PMID:12373019. |
endochondral ossification requires coordinated maturation, proliferation and differentiation of growth plate chondrocytes leading to hypertrophic cells which eventually undergo apoptosis to leave a cartilaginous scaffold that is mineralized prior to the laying down of new bone. |
2003-03-17 |
2023-08-12 |
Not clear |
| Jeffrey F Waring, Rebecca Gum, David Morfitt, Robert A Jolly, Rita Ciurlionis, Matthew Heindel, Lori Gallenberg, Bruno Buratto, Roger G Ulric. Identifying toxic mechanisms using DNA microarrays: evidence that an experimental inhibitor of cell adhesion molecule expression signals through the aryl hydrocarbon nuclear receptor. Toxicology. vol 181-182. 2003-02-28. PMID:12505364. |
in addition, several genes involved in apoptosis and cell cycle were differentially expressed consistent with cell turnover, hypertrophy and hyperplasia observed by histology. |
2003-02-28 |
2023-08-12 |
rat |
| J J Miguel-Hidalgo, X A Alvarez, R Cacabelos, G Quac. Neuroprotection by memantine against neurodegeneration induced by beta-amyloid(1-40). Brain research. vol 958. issue 1. 2003-02-25. PMID:12468047. |
abeta(1-40), but not water, injections into hippocampus led to neuronal loss in the ca1 subfield, evidence of widespread apoptosis, and astrocytic and microglial activation and hypertrophy. |
2003-02-25 |
2023-08-12 |
rat |
| J Lu, J Xiao, H Luo, H Che. [Apoptosis in pressure overload-induced heart hypertrophy]. Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi. vol 18. issue 2. 2003-02-20. PMID:11450537. |
[apoptosis in pressure overload-induced heart hypertrophy]. |
2003-02-20 |
2023-08-12 |
rat |
| J Lu, J Xiao, H Luo, H Che. [Apoptosis in pressure overload-induced heart hypertrophy]. Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi. vol 18. issue 2. 2003-02-20. PMID:11450537. |
pressure overload can result in heart hypertrophy, and induce apoptosis, but the phenomenon of apoptosis during the forepart of cardiomyocyte hypertrophy remains unclear. |
2003-02-20 |
2023-08-12 |
rat |
| J Lu, J Xiao, H Luo, H Che. [Apoptosis in pressure overload-induced heart hypertrophy]. Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi. vol 18. issue 2. 2003-02-20. PMID:11450537. |
the aim of this study was to inquire into the process of cardiomyocyte apoptosis during the forepart of cardiomyocyte hypertrophy. |
2003-02-20 |
2023-08-12 |
rat |
| J Lu, J Xiao, H Luo, H Che. [Apoptosis in pressure overload-induced heart hypertrophy]. Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi. vol 18. issue 2. 2003-02-20. PMID:11450537. |
these data indicate that cardiac hypertrophy is initiated by apoptosis of cardiomyocyte, these two factors(hypertrophy and apoptosis) maintain the balance between growth and death during the early short period of aortic constriction, and when aortic constriction goes on they are involved in the pathogenesis of heart remodeling. |
2003-02-20 |
2023-08-12 |
rat |
| Annarosa Leri, Sonia Franco, Antonella Zacheo, Laura Barlucchi, Stefano Chimenti, Federica Limana, Bernardo Nadal-Ginard, Jan Kajstura, Piero Anversa, María A Blasc. Ablation of telomerase and telomere loss leads to cardiac dilatation and heart failure associated with p53 upregulation. The EMBO journal. vol 22. issue 1. 2003-02-12. PMID:12505991. |
telomere shortening in g2 and g5 terc-/- mice was coupled with attenuation in cardiac myocyte proliferation, increased apoptosis and cardiac myocyte hypertrophy. |
2003-02-12 |
2023-08-12 |
mouse |
| Mehran Mandegar, Jason X J Yua. Role of K+ channels in pulmonary hypertension. Vascular pharmacology. vol 38. issue 1. 2003-01-15. PMID:12378819. |
dysfunction of k+ channels has also been linked to decreased apoptosis in pulmonary arterial smcs, a condition that contributes further to the medial hypertrophy of the arterial walls and vascular remodeling. |
2003-01-15 |
2023-08-12 |
Not clear |