All Relations between apoptosis and hypertrophic

Publication Sentence Publish Date Extraction Date Species
J Hegarty, R N Fole. Anaemia, renal insufficiency and cardiovascular outcome. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. vol 16 Suppl 1. 2001-08-23. PMID:11369834. cellular models of cardiac hypertrophy and cardiac failure suggest that haemodynamic stresses lead to increased rates of cardiac myocyte apoptosis and fibrosis. 2001-08-23 2023-08-12 Not clear
B C Ber. Vascular smooth muscle growth: autocrine growth mechanisms. Physiological reviews. vol 81. issue 3. 2001-07-26. PMID:11427690. vascular smooth muscle cells (vsmc) exhibit several growth responses to agonists that regulate their function including proliferation (hyperplasia with an increase in cell number), hypertrophy (an increase in cell size without change in dna content), endoreduplication (an increase in dna content and usually size), and apoptosis. 2001-07-26 2023-08-12 Not clear
K C Wollert, H Drexle. The role of interleukin-6 in the failing heart. Heart failure reviews. vol 6. issue 2. 2001-07-12. PMID:11309528. experimental studies have produced compelling evidence that il-6 and il-6 related cytokines play a pivotal role in the regulation of cardiac myocyte hypertrophy and apoptosis. 2001-07-12 2023-08-12 Not clear
M Zeisberg, F Strutz, G A Mülle. Renal fibrosis: an update. Current opinion in nephrology and hypertension. vol 10. issue 3. 2001-07-12. PMID:11342792. whereas tubular epithelial cells react by proliferation or hypertrophy to initial stimuli, they may undergo apoptosis or transdifferentiate into fibroblasts, and thus contribute to tubular atrophy in later stages of progressive renal disease. 2001-07-12 2023-08-12 Not clear
C Shan. Electrophysiology of growth control and acupuncture. Life sciences. vol 68. issue 12. 2001-06-21. PMID:11388686. the regulation of most physiological processes is through growth control mechanisms such as hypertrophy, hyperplasia, atrophy, and apoptosis. 2001-06-21 2023-08-12 Not clear
K Mansfield, C C Teixeira, C S Adams, I M Shapir. Phosphate ions mediate chondrocyte apoptosis through a plasma membrane transporter mechanism. Bone. vol 28. issue 1. 2001-06-07. PMID:11165936. in a previous investigation we showed that phosphate ions (pi) induced apoptosis of terminally differentiated hypertrophic chondrocytes. 2001-06-07 2023-08-12 chicken
C M Alexander, S Selvarajan, J Mudgett, Z Wer. Stromelysin-1 regulates adipogenesis during mammary gland involution. The Journal of cell biology. vol 152. issue 4. 2001-05-21. PMID:11266461. 135:1669-1677), we found that during post-lactational involution, mammary glands from transgenic mice that overexpress the tissue inhibitor of metalloproteinases, timp-1 (to), or mice carrying a targeted mutation in str1 showed accelerated differentiation and hypertrophy of adipocytes, while epithelial apoptosis was unaffected. 2001-05-21 2023-08-12 mouse
H P Gerber, N Ferrar. Angiogenesis and bone growth. Trends in cardiovascular medicine. vol 10. issue 5. 2001-05-21. PMID:11282299. recent experimental findings provide an explanation why the close proximity of cartilage and vasculature is mutually exclusive: vascular invasion of cartilage is associated with chondrocyte apoptosis and consequently, inhibition of angiogenesis in the growth plate delays chondrocyte cell death, resulting in a massive expansion in the number of hypertrophic cartilage cells in the growth plate. 2001-05-21 2023-08-12 Not clear
X Yang, L Chen, X Xu, C Li, C Huang, C X Den. TGF-beta/Smad3 signals repress chondrocyte hypertrophic differentiation and are required for maintaining articular cartilage. The Journal of cell biology. vol 153. issue 1. 2001-05-21. PMID:11285272. the cartilage then goes through a program of cell proliferation, hypertrophic differentiation, calcification, apoptosis, and eventually is replaced by bone. 2001-05-21 2023-08-12 mouse
J W Adams, J H Brow. G-proteins in growth and apoptosis: lessons from the heart. Oncogene. vol 20. issue 13. 2001-05-10. PMID:11313910. cardiomyocytes provide an ideal model system for understanding the basis for g-protein mediated hypertrophy and apoptosis, and the mechanisms responsible for the transition from compensatory to deleterious levels of signaling. 2001-05-10 2023-08-12 mouse
T Omura, M Yoshiyama, F Ishikura, H Kobayashi, K Takeuchi, S Beppu, J Yoshikaw. Myocardial ischemia activates the JAK-STAT pathway through angiotensin II signaling in in vivo myocardium of rats. Journal of molecular and cellular cardiology. vol 33. issue 2. 2001-04-26. PMID:11162135. as the signal transduction pathway responsible for myocardial hypertrophy and apoptosis, janus kinase (jak) and signal transducers and activators of transcription (stat) are suggested to play an important role. 2001-04-26 2023-08-12 rat
G A Karpouzas, R A Terkeltau. New developments in the pathogenesis of articular cartilage calcification. Current rheumatology reports. vol 1. issue 2. 2001-03-29. PMID:11123025. these include chondrocyte proliferation, hypertrophy and increased apoptosis. 2001-03-29 2023-08-12 Not clear
R Pochampally, C Li, W Lu, L Chen, R Luftig, J Lin, J Che. Temperature-sensitive mutants of p53 homologs. Biochemical and biophysical research communications. vol 279. issue 3. 2001-03-29. PMID:11162465. activation of p73beta-ile156 in h1299 cells inhibits cell division but induces significant increase in cell size (hypertrophy), whereas activation of p73alpha-leu156 and p63gamma-pro167 induces apoptosis. 2001-03-29 2023-08-12 Not clear
H Jänkälä, K K Eklund, J O Kokkonen, P T Kovanen, K A Linstedt, M Härkönen, T Mäk. Ethanol infusion increases ANP and p21 gene expression in isolated perfused rat heart. Biochemical and biophysical research communications. vol 281. issue 2. 2001-03-29. PMID:11181050. we conclude that ethanol per se is capable of inducing genes associated with hypertrophy and impaired function of the heart whereas a significant apoptosis is not involved in the initial phase of alcohol-induced cardiac injury. 2001-03-29 2023-08-12 rat
M Zenmyo, S Komiya, T Hamada, K Hiraoka, R Suzuki, A Inou. p21 and parathyroid hormone-related peptide in the growth plate. Calcified tissue international. vol 67. issue 5. 2001-03-22. PMID:11136536. we have previously demonstrated that apoptosis occurred in the terminal hypertrophic chondrocyte of the growth plate. 2001-03-22 2023-08-12 Not clear
b' J Morisset, S Morisset, K Lauzon, S C\\xc3\\xb4t\\xc3\\xa9, J Lain\\xc3\\xa9, J Bourassa, M Lessard, V Echav\\xc3\\xa. Pancreatic inflammation, apoptosis, and growth: sequential events after partial pancreatectomy in pigs. Pancreas. vol 21. issue 3. 2001-02-01. PMID:11039478.' this study was undertaken to establish the time course of pancreatic inflammation, apoptosis, and hypertrophy and/or hyperplasia after partial pancreatectomy in pigs. 2001-02-01 2023-08-12 human
C C Shieh, M Coghlan, J P Sullivan, M Gopalakrishna. Potassium channels: molecular defects, diseases, and therapeutic opportunities. Pharmacological reviews. vol 52. issue 4. 2001-01-04. PMID:11121510. in addition, changes in k(+) channel function have been associated with cardiac hypertrophy and failure, apoptosis and oncogenesis, and various neurodegenerative and neuromuscular disorders. 2001-01-04 2023-08-12 human
N G Kavantzas, A C Lazaris, E V Agapitos, J Nanas, P S Davari. Histological assessment of apoptotic cell death in cardiomyopathies. Pathology. vol 32. issue 3. 2000-12-22. PMID:10968390. in the present study, we describe the amount of apoptosis in 50 endomyocardial biopsies taken from 50 patients with dilated cardiomyopathy, in 14 hearts with hypertrophic cardiomyopathy and in five hearts with arrhythmogenic dysplasia of the right ventricle. 2000-12-22 2023-08-12 human
T Chodon, T Sugihara, H H Igawa, E Funayama, H Furukaw. Keloid-derived fibroblasts are refractory to Fas-mediated apoptosis and neutralization of autocrine transforming growth factor-beta1 can abrogate this resistance. The American journal of pathology. vol 157. issue 5. 2000-12-07. PMID:11073825. here, we report that in contrast to hypertrophic scar-derived and normal skin-derived fibroblasts, keloid-derived fibroblasts are significantly resistant to both fas-mediated and staurosporine-induced apoptosis. 2000-12-07 2023-08-12 Not clear
T Chodon, T Sugihara, H H Igawa, E Funayama, H Furukaw. Keloid-derived fibroblasts are refractory to Fas-mediated apoptosis and neutralization of autocrine transforming growth factor-beta1 can abrogate this resistance. The American journal of pathology. vol 157. issue 5. 2000-12-07. PMID:11073825. there were no significant differences in the level of expression of fas, bcl-2, and bax between the three groups but addition of transforming growth factor (tgf)-beta1 significantly inhibited fas-mediated apoptosis in hypertrophic scar-derived and normal skin-derived fibroblasts and neutralization of autocrine tgf-beta1 with anti-tgf-beta1 antibody abrogated the resistance of keloid-derived fibroblasts. 2000-12-07 2023-08-12 Not clear