| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Abdelkarim Sabri, Brenda A Wilson, Susan F Steinber. Dual actions of the Galpha(q) agonist Pasteurella multocida toxin to promote cardiomyocyte hypertrophy and enhance apoptosis susceptibility. Circulation research. vol 90. issue 8. 2002-05-14. PMID:11988485. |
dual actions of the galpha(q) agonist pasteurella multocida toxin to promote cardiomyocyte hypertrophy and enhance apoptosis susceptibility. |
2002-05-14 |
2023-08-12 |
mouse |
| Abdelkarim Sabri, Brenda A Wilson, Susan F Steinber. Dual actions of the Galpha(q) agonist Pasteurella multocida toxin to promote cardiomyocyte hypertrophy and enhance apoptosis susceptibility. Circulation research. vol 90. issue 8. 2002-05-14. PMID:11988485. |
modest levels of wild-type galpha(q) overexpression induce stable cardiac hypertrophy, whereas intense galpha(q) stimulation induces cardiomyocyte apoptosis. |
2002-05-14 |
2023-08-12 |
mouse |
| Abdelkarim Sabri, Brenda A Wilson, Susan F Steinber. Dual actions of the Galpha(q) agonist Pasteurella multocida toxin to promote cardiomyocyte hypertrophy and enhance apoptosis susceptibility. Circulation research. vol 90. issue 8. 2002-05-14. PMID:11988485. |
the precise mechanism(s) whereby traditional targets of galpha (q) subunits that induce hypertrophy also trigger cardiomyocyte apoptosis is not obvious and is explored with recombinant pasteurella multocida toxin (rpmt, a galpha(q) agonist). |
2002-05-14 |
2023-08-12 |
mouse |
| Abdelkarim Sabri, Brenda A Wilson, Susan F Steinber. Dual actions of the Galpha(q) agonist Pasteurella multocida toxin to promote cardiomyocyte hypertrophy and enhance apoptosis susceptibility. Circulation research. vol 90. issue 8. 2002-05-14. PMID:11988485. |
because inhibition of akt enhances cardiomyocyte susceptibility to apoptosis, this pathway is predicted to contribute to the transition from hypertrophy to cardiac decompensation and could be targeted for therapy in heart failure. |
2002-05-14 |
2023-08-12 |
mouse |
| V A Frolov, G A Drozdova, V F Mustyatsa, P Rieger, Z Antoni, A E Kuzovki. Possible mechanism of regression of myocardial hypertrophy. Bulletin of experimental biology and medicine. vol 132. issue 1. 2002-05-07. PMID:11687842. |
regression of hypertrophic changes was accompanied by a marked increase in the number of extracellular nuclei, which indicated enhanced apoptosis of cardiomyocytes. |
2002-05-07 |
2023-08-12 |
Not clear |
| Weimin Li, Ningling Sun, Wei Liu, Yuanyuan Chen, Youzhi Y. Influence of Valsartan on myocardial apoptosis in spontaneously hypertensive rats. Chinese medical journal. vol 115. issue 3. 2002-05-01. PMID:11940365. |
to explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of valsartan. |
2002-05-01 |
2023-08-12 |
rat |
| Y Akasaka, K Fujita, Y Ishikawa, N Asuwa, K Inuzuka, M Ishihara, M Ito, T Masuda, Y Akishima, L Zhang, K Ito, T Ishi. Detection of apoptosis in keloids and a comparative study on apoptosis between keloids, hypertrophic scars, normal healed flat scars, and dermatofibroma. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. vol 9. issue 6. 2002-04-26. PMID:11896992. |
detection of apoptosis in keloids and a comparative study on apoptosis between keloids, hypertrophic scars, normal healed flat scars, and dermatofibroma. |
2002-04-26 |
2023-08-12 |
Not clear |
| Y Akasaka, K Fujita, Y Ishikawa, N Asuwa, K Inuzuka, M Ishihara, M Ito, T Masuda, Y Akishima, L Zhang, K Ito, T Ishi. Detection of apoptosis in keloids and a comparative study on apoptosis between keloids, hypertrophic scars, normal healed flat scars, and dermatofibroma. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. vol 9. issue 6. 2002-04-26. PMID:11896992. |
to further reveal the phenomenon of apoptosis, we quantified the number of terminal deoxynucleotide transferase-mediated dutp nick-end labeling (tunel)-positive cells in surgically resected tissues of keloids (n = 10), hypertrophic scars (n = 10), normal healed flat scars (n = 10), and dermatofibroma (n = 10). |
2002-04-26 |
2023-08-12 |
Not clear |
| Y Akasaka, K Fujita, Y Ishikawa, N Asuwa, K Inuzuka, M Ishihara, M Ito, T Masuda, Y Akishima, L Zhang, K Ito, T Ishi. Detection of apoptosis in keloids and a comparative study on apoptosis between keloids, hypertrophic scars, normal healed flat scars, and dermatofibroma. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. vol 9. issue 6. 2002-04-26. PMID:11896992. |
hypertrophic scars had significantly higher levels of apoptosis than normally healed flat scars (p = 0.033). |
2002-04-26 |
2023-08-12 |
Not clear |
| Y Akasaka, K Fujita, Y Ishikawa, N Asuwa, K Inuzuka, M Ishihara, M Ito, T Masuda, Y Akishima, L Zhang, K Ito, T Ishi. Detection of apoptosis in keloids and a comparative study on apoptosis between keloids, hypertrophic scars, normal healed flat scars, and dermatofibroma. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. vol 9. issue 6. 2002-04-26. PMID:11896992. |
therefore, these results suggest that selected fibroblasts in keloids and hypertrophic scars undergo apoptosis, which may play a role in the process of pathological scarring. |
2002-04-26 |
2023-08-12 |
Not clear |
| A L Boskey, E P Paschalis, I Binderman, S B Dot. BMP-6 accelerates both chondrogenesis and mineral maturation in differentiating chick limb-bud mesenchymal cell cultures. Journal of cellular biochemistry. vol 84. issue 3. 2002-03-19. PMID:11813256. |
these hypertrophic chondrocytes are characterized by their increased expression of type x collagen, alkaline phosphatase activity, and apoptosis, as well as by the ability of their extracellular matrices to support mineral deposition. |
2002-03-19 |
2023-08-12 |
chicken |
| Cornel Badorff, Hartmut Ruetten, Sven Mueller, Meike Stahmer, Doris Gehring, Frank Jung, Christian Ihling, Andreas M Zeiher, Stefanie Dimmele. Fas receptor signaling inhibits glycogen synthase kinase 3 beta and induces cardiac hypertrophy following pressure overload. The Journal of clinical investigation. vol 109. issue 3. 2002-03-06. PMID:11827997. |
here, we identified fas receptor activation, a classical death signal causing apoptosis via activation of the caspase cascade in many cell types, as a novel pathway mediating cardiomyocyte hypertrophy in vitro and in vivo. |
2002-03-06 |
2023-08-12 |
mouse |
| Luigi Matturri, José Milei, Daniel Rodolfo Grana, Anna Maria Lavezz. Characterization of myocardial hypertrophy by DNA content, PCNA expression and apoptotic index. International journal of cardiology. vol 82. issue 1. 2002-03-05. PMID:11786155. |
the present study aims to analyze proliferating cell nuclear antigen (pcna) expression, dna content and apoptosis, in several types of myocardial hypertrophy in order to define the biological characteristics of this process. |
2002-03-05 |
2023-08-12 |
Not clear |
| Thomas Force, Syed Haq, Heiko Kilter, Ashour Michae. Apoptosis signal-regulating kinase/nuclear factor-kappaB: a novel signaling pathway regulates cardiomyocyte hypertrophy. Circulation. vol 105. issue 4. 2002-02-12. PMID:11815417. |
apoptosis signal-regulating kinase/nuclear factor-kappab: a novel signaling pathway regulates cardiomyocyte hypertrophy. |
2002-02-12 |
2023-08-12 |
Not clear |
| Shinichi Hirotani, Kinya Otsu, Kazuhiko Nishida, Yoshiharu Higuchi, Takashi Morita, Hiroyuki Nakayama, Osamu Yamaguchi, Toshiaki Mano, Yasushi Matsumura, Hikaru Ueno, Michihiko Tada, Masatsugu Hor. Involvement of nuclear factor-kappaB and apoptosis signal-regulating kinase 1 in G-protein-coupled receptor agonist-induced cardiomyocyte hypertrophy. Circulation. vol 105. issue 4. 2002-02-12. PMID:11815436. |
involvement of nuclear factor-kappab and apoptosis signal-regulating kinase 1 in g-protein-coupled receptor agonist-induced cardiomyocyte hypertrophy. |
2002-02-12 |
2023-08-12 |
rat |
| Shinichi Hirotani, Kinya Otsu, Kazuhiko Nishida, Yoshiharu Higuchi, Takashi Morita, Hiroyuki Nakayama, Osamu Yamaguchi, Toshiaki Mano, Yasushi Matsumura, Hikaru Ueno, Michihiko Tada, Masatsugu Hor. Involvement of nuclear factor-kappaB and apoptosis signal-regulating kinase 1 in G-protein-coupled receptor agonist-induced cardiomyocyte hypertrophy. Circulation. vol 105. issue 4. 2002-02-12. PMID:11815436. |
in this study, we examined the role of an ros-sensitive transcriptional factor, nf-kappab, and a mitogen-activated protein kinase kinase kinase, apoptosis signal-regulating kinase 1 (ask1), in g-protein-coupled receptor (gpcr) agonist (angiotensin ii, endothelin-1, phenylephrine)-induced cardiac hypertrophy in isolated rat neonatal cardiomyocytes. |
2002-02-12 |
2023-08-12 |
rat |
| G Yu, X Liang, X Xie, M Su, S Zha. Diverse effects of chronic treatment with losartan, fosinopril, and amlodipine on apoptosis, angiotensin II in the left ventricle of hypertensive rats. International journal of cardiology. vol 81. issue 2-3. 2002-01-31. PMID:11744126. |
the results of this study indicate that losartan, fosinopril, and amlodipine each effectively reverses heart hypertrophy and inhibits cardiomyocyte apoptosis, and fosinopril may be most effective in these cardioprotective effects. |
2002-01-31 |
2023-08-12 |
rat |
| G Yu, X Liang, X Xie, M Su, S Zha. Diverse effects of chronic treatment with losartan, fosinopril, and amlodipine on apoptosis, angiotensin II in the left ventricle of hypertensive rats. International journal of cardiology. vol 81. issue 2-3. 2002-01-31. PMID:11744126. |
these findings suggest that the effects of the three blockers on myocardiocyte apoptosis and left ventricular hypertrophy were related to inhibition of the myocardium rennin-angiotensin-aldsterone system. |
2002-01-31 |
2023-08-12 |
rat |
| T Yamauchi, T Kadowak. [The molecular mechanisms by which PPAR gamma/RXR inhibitors improve insulin resistance]. Nihon rinsho. Japanese journal of clinical medicine. vol 59. issue 11. 2002-01-25. PMID:11712415. |
moreover, ppar gamma/rxr inhibitors decrease lipogenesis in wat, while tzd stimulate adipocyte differentiation and apoptosis, thereby both preventing adipocyte hypertrophy, which is associated with alleviation of insulin resistance presumably due to decreases in ffa, and tnf alpha, and upregulation of adiponectin. |
2002-01-25 |
2023-08-12 |
Not clear |
| K Singh, L Xiao, A Remondino, D B Sawyer, W S Colucc. Adrenergic regulation of cardiac myocyte apoptosis. Journal of cellular physiology. vol 189. issue 3. 2002-01-03. PMID:11748583. |
the direct effects of catecholamines on cardiac myocytes may contribute to both normal physiologic adaptation and pathologic remodeling, and may be associated with cellular hypertrophy, apoptosis, and alterations in contractile function. |
2002-01-03 |
2023-08-12 |
mouse |