All Relations between apoptosis and hypertrophic

Publication Sentence Publish Date Extraction Date Species
Tsutomu Yoshikaw. [Alterations in sympathoadrenal system in congestive heart failure]. Nihon rinsho. Japanese journal of clinical medicine. vol 61. issue 5. 2003-08-08. PMID:12754996. mechanisms underlying such adverse effects involve multiple biological events including production of oxygen free radicals, cytokines, matrix metalloproteinase, apoptosis, cardiac hypertrophy, and chamber remodeling as well as energy expenditure. 2003-08-08 2023-08-12 mouse
b' M Strniskov\\xc3\\xa1, M Baranc\\xc3\\xadk, T Ravingerov\\xc3\\xa. Mitogen-activated protein kinases and their role in regulation of cellular processes. General physiology and biophysics. vol 21. issue 3. 2003-08-04. PMID:12537349.' this paper is focused on characterization of these mapk cascades in terms of their distribution and biological role in some pathological processes (apoptosis, hypertrophy) with a special orientation on the role of mapks in cardiovascular system during ischemia/reperfusion. 2003-08-04 2023-08-12 Not clear
E Grimaud, F Blanchard, C Charrier, F Gouin, F Redini, D Heyman. Leukaemia inhibitory factor (lif) is expressed in hypertrophic chondrocytes and vascular sprouts during osteogenesis. Cytokine. vol 20. issue 5. 2003-08-01. PMID:12550107. avascular cartilage is replaced by highly vascularized bone tissue during endochondral ossification, a process involving capillary invasion of calcified hypertrophic cartilage in association with apoptosis of hypertrophic chondrocytes, degradation of cartilage matrix and deposition of bone matrix. 2003-08-01 2023-08-12 human
Nathalie Ortega, Danielle Behonick, Dominique Stickens, Zena Wer. How proteases regulate bone morphogenesis. Annals of the New York Academy of Sciences. vol 995. 2003-07-22. PMID:12814943. apoptosis of the terminal hypertrophic chondrocytes, degradation of the cartilage matrix, and deposition of bone matrix by osteoblasts accompanies neovascularization of the growth plate. 2003-07-22 2023-08-12 mouse
Yoshiharu Higuchi, Kinya Otsu, Kazuhiko Nishida, Shinichi Hirotani, Hiroyuki Nakayama, Osamu Yamaguchi, Shungo Hikoso, Kazunori Kashiwase, Toshihiro Takeda, Tetsuya Watanabe, Toshiaki Mano, Yasushi Matsumura, Hikaru Ueno, Masatsugu Hor. The small GTP-binding protein Rac1 induces cardiac myocyte hypertrophy through the activation of apoptosis signal-regulating kinase 1 and nuclear factor-kappa B. The Journal of biological chemistry. vol 278. issue 23. 2003-07-18. PMID:12672819. the small gtp-binding protein rac1 induces cardiac myocyte hypertrophy through the activation of apoptosis signal-regulating kinase 1 and nuclear factor-kappa b. 2003-07-18 2023-08-12 Not clear
Yoshiharu Higuchi, Kinya Otsu, Kazuhiko Nishida, Shinichi Hirotani, Hiroyuki Nakayama, Osamu Yamaguchi, Shungo Hikoso, Kazunori Kashiwase, Toshihiro Takeda, Tetsuya Watanabe, Toshiaki Mano, Yasushi Matsumura, Hikaru Ueno, Masatsugu Hor. The small GTP-binding protein Rac1 induces cardiac myocyte hypertrophy through the activation of apoptosis signal-regulating kinase 1 and nuclear factor-kappa B. The Journal of biological chemistry. vol 278. issue 23. 2003-07-18. PMID:12672819. recently, we reported on apoptosis signal-regulating kinase (ask) 1 and a transcriptional factor, nuclear factor-kappab (nf-kappab), as novel signaling intermediates in cardiac myocyte hypertrophy. 2003-07-18 2023-08-12 Not clear
J A Byrne, D J Grieve, A C Cave, A M Sha. Oxidative stress and heart failure. Archives des maladies du coeur et des vaisseaux. vol 96. issue 3. 2003-07-15. PMID:12722552. as well as direct effects on cellular enzymatic and protein function, ros have been implicated in the development of agonist-induced cardiac hypertrophy, cardiomyocyte apoptosis and remodelling of the failing myocardium. 2003-07-15 2023-08-12 Not clear
Yang Xiang, Brian K Kobilk. Myocyte adrenoceptor signaling pathways. Science (New York, N.Y.). vol 300. issue 5625. 2003-06-26. PMID:12791980. however, in heart failure, chronic catecholamine stimulation of adrenoceptors has been linked to pathologic cardiac remodeling, including myocyte apoptosis and hypertrophy. 2003-06-26 2023-08-12 Not clear
Suyang Tang, Baoren Cai, Huorong Xu, Huiyuan Li, Shuzhong Guo, Li Yang, Binglun Lu, Linxi Zhan. [The influence of Matrine on apoptosis of fibroblasts and the expression of apoptotic modulation related protein in hypertrophic scar of rabbit ear]. Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns. vol 18. issue 5. 2003-06-12. PMID:12515645. [the influence of matrine on apoptosis of fibroblasts and the expression of apoptotic modulation related protein in hypertrophic scar of rabbit ear]. 2003-06-12 2023-08-12 rabbit
Suyang Tang, Baoren Cai, Huorong Xu, Huiyuan Li, Shuzhong Guo, Li Yang, Binglun Lu, Linxi Zhan. [The influence of Matrine on apoptosis of fibroblasts and the expression of apoptotic modulation related protein in hypertrophic scar of rabbit ear]. Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns. vol 18. issue 5. 2003-06-12. PMID:12515645. to investigate the effects of matrine on apoptosis of fibroblasts and the expression of apoptotic modulation related protein in the hypertrophic scar. 2003-06-12 2023-08-12 rabbit
Nikesh Thiruchelvam, Peter Nyirady, Donald M Peebles, Christopher H Fry, Peter M Cuckow, Adrian S Wool. Urinary outflow obstruction increases apoptosis and deregulates Bcl-2 and Bax expression in the fetal ovine bladder. The American journal of pathology. vol 162. issue 4. 2003-06-12. PMID:12651619. we speculate that enhanced apoptosis in detrusor smooth muscle cells is part of a remodeling response during compensatory hyperplasia and hypertrophy. 2003-06-12 2023-08-12 human
Kai C Wollert, Helmut Drexle. Regulation of cardiac remodeling by nitric oxide: focus on cardiac myocyte hypertrophy and apoptosis. Heart failure reviews. vol 7. issue 4. 2003-06-04. PMID:12379817. regulation of cardiac remodeling by nitric oxide: focus on cardiac myocyte hypertrophy and apoptosis. 2003-06-04 2023-08-12 mouse
Kai C Wollert, Helmut Drexle. Regulation of cardiac remodeling by nitric oxide: focus on cardiac myocyte hypertrophy and apoptosis. Heart failure reviews. vol 7. issue 4. 2003-06-04. PMID:12379817. a prevailing concept predicts that changes in gene expression in hypertrophied cardiac myocytes and cardiac myocyte loss by apoptosis contribute to the transition from hypertrophy to failure. 2003-06-04 2023-08-12 mouse
Suresh C Tyagi, Brian D Hoi. Metalloproteinase in myocardial adaptation and maladaptation. Journal of cardiovascular pharmacology and therapeutics. vol 7. issue 4. 2003-06-04. PMID:12490970. ventricular remodeling is a compensatory response that comprises the processes of apoptosis, muscle cell hypertrophy, and rearrangement of the extracellular matrix fibers connecting the muscles. 2003-06-04 2023-08-12 Not clear
Suresh C Tyagi, Brian D Hoi. Metalloproteinase in myocardial adaptation and maladaptation. Journal of cardiovascular pharmacology and therapeutics. vol 7. issue 4. 2003-06-04. PMID:12490970. however, a complete extracellular matrix-cell disconnect leads to a decrease in muscle cell strength, apoptosis, and hypertrophy. 2003-06-04 2023-08-12 Not clear
Pål Aukrust, Jan Kristian Damås, Lars Gullesta. Immunomodulating therapy: new treatment modality in congestive heart failure. Congestive heart failure (Greenwich, Conn.). vol 9. issue 2. 2003-06-04. PMID:12671336. accumulating evidence indicates that inflammatory cytokines play a pathogenic role in congestive heart failure (chf) by influencing heart contractility, inducing hypertrophy, and promoting apoptosis or fibrosis, contributing to the continuous myocardial remodeling process. 2003-06-04 2023-08-12 Not clear
Shimako Yamamoto, Guiping Yang, Daniela Zablocki, Jing Liu, Chull Hong, Song-Jung Kim, Sandra Soler, Mari Odashima, Jill Thaisz, Ghassan Yehia, Carlos A Molina, Atsuko Yatani, Dorothy E Vatner, Stephen F Vatner, Junichi Sadoshim. Activation of Mst1 causes dilated cardiomyopathy by stimulating apoptosis without compensatory ventricular myocyte hypertrophy. The Journal of clinical investigation. vol 111. issue 10. 2003-06-04. PMID:12750396. activation of mst1 causes dilated cardiomyopathy by stimulating apoptosis without compensatory ventricular myocyte hypertrophy. 2003-06-04 2023-08-12 mouse
Shimako Yamamoto, Guiping Yang, Daniela Zablocki, Jing Liu, Chull Hong, Song-Jung Kim, Sandra Soler, Mari Odashima, Jill Thaisz, Ghassan Yehia, Carlos A Molina, Atsuko Yatani, Dorothy E Vatner, Stephen F Vatner, Junichi Sadoshim. Activation of Mst1 causes dilated cardiomyopathy by stimulating apoptosis without compensatory ventricular myocyte hypertrophy. The Journal of clinical investigation. vol 111. issue 10. 2003-06-04. PMID:12750396. these results show that mst1 works as both an essential initiator of apoptosis and an inhibitor of hypertrophy in cardiac myocytes, resulting in a previously unrecognized form of cardiomyopathy. 2003-06-04 2023-08-12 mouse
Arnold M Kat. Proliferative signaling and disease progression in heart failure. Circulation journal : official journal of the Japanese Circulation Society. vol 66. issue 3. 2003-06-03. PMID:11922268. these findings can be explained by crossovers between functional and proliferative signaling, among the most important of which is the ability of neurohumoral mediators, such as norepinephrine and angiotensin ii, to stimulate maladaptive hypertrophy, remodeling, apoptosis and other deleterious proliferative responses in the failing heart. 2003-06-03 2023-08-12 Not clear
Marion Persoon-Rothert, Karlien G C van der Wees, Arnoud van der Laars. Mechanical overload-induced apoptosis: a study in cultured neonatal ventricular myocytes and fibroblasts. Molecular and cellular biochemistry. vol 241. issue 1-2. 2003-05-28. PMID:12482033. reports on the role of apoptosis in the transition from hypertrophy to decompensated heart failure are not unequivocal. 2003-05-28 2023-08-12 rat