| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Bing Feng, Wei Liu, Jing Xu, Zuo-Yun He, Hui-Biao Yan. [Relationship between apoptosis and alteration of the energetic metabolism pathways of hypertrophic cardiomyocytes induced by hypoxia-reoxygenation]. Sheng li xue bao : [Acta physiologica Sinica]. vol 57. issue 5. 2013-12-05. PMID:16220203. |
this study focused on the relationship between apoptosis and alteration of the energetic metabolism pathways of hypertrophic cardiomyocytes induced by hypoxia-reoxygenation. |
2013-12-05 |
2023-08-12 |
Not clear |
| Bing Feng, Wei Liu, Jing Xu, Zuo-Yun He, Hui-Biao Yan. [Relationship between apoptosis and alteration of the energetic metabolism pathways of hypertrophic cardiomyocytes induced by hypoxia-reoxygenation]. Sheng li xue bao : [Acta physiologica Sinica]. vol 57. issue 5. 2013-12-05. PMID:16220203. |
(5) the rate of apoptosis in hypertrophic cardiocytes increased obviously after hypoxia for 8 h, and increased further and markedly at the early stage of reoxygenation, then gradually decreased to normal level. |
2013-12-05 |
2023-08-12 |
Not clear |
| Bing Feng, Wei Liu, Jing Xu, Zuo-Yun He, Hui-Biao Yan. [Relationship between apoptosis and alteration of the energetic metabolism pathways of hypertrophic cardiomyocytes induced by hypoxia-reoxygenation]. Sheng li xue bao : [Acta physiologica Sinica]. vol 57. issue 5. 2013-12-05. PMID:16220203. |
(6) dicholoroacetate could inhibit apoptosis of hypertrophic cardiocytes through increasing glucose oxidation and inhibiting the activation of glycolysis and fatty acid oxidation of hypertrophic cardiomyocytes induced by hypoxia-reoxygenation. |
2013-12-05 |
2023-08-12 |
Not clear |
| Bing Feng, Wei Liu, Jing Xu, Zuo-Yun He, Hui-Biao Yan. [Relationship between apoptosis and alteration of the energetic metabolism pathways of hypertrophic cardiomyocytes induced by hypoxia-reoxygenation]. Sheng li xue bao : [Acta physiologica Sinica]. vol 57. issue 5. 2013-12-05. PMID:16220203. |
these data demonstrate that apoptosis in hypertrophic cardiomyocytes after hypoxia-reoxygenation is mainly due to the inhibition of glucose oxidation and the activation of glucolysis and fatty acid oxidation. |
2013-12-05 |
2023-08-12 |
Not clear |
| Bing Feng, Wei Liu, Jing Xu, Zuo-Yun He, Hui-Biao Yan. [Relationship between apoptosis and alteration of the energetic metabolism pathways of hypertrophic cardiomyocytes induced by hypoxia-reoxygenation]. Sheng li xue bao : [Acta physiologica Sinica]. vol 57. issue 5. 2013-12-05. PMID:16220203. |
furthermore, increasing glucose oxidation may be a new pharmacotherapeutic target to inhibit apoptosis of hypertrophic cardiac cells. |
2013-12-05 |
2023-08-12 |
Not clear |
| Huali Chen, Xue Wang, Mingming Tong, Dan Wu, Sisi Wu, Jiaxiang Chen, Xiaoxiao Wang, Xulei Wang, Yu Kang, Hong Tang, Chaoshu Tang, Wei Jian. Intermedin suppresses pressure overload cardiac hypertrophy through activation of autophagy. PloS one. vol 8. issue 5. 2013-11-25. PMID:23737997. |
furthermore, the heart size, heart weight/body weight ratios, cardiomyocyte size and apoptosis, interstitial collagen, hypertrophic markers including anp and bnp expression were also significantly increased, which were effectively suppressed by imd supplementation. |
2013-11-25 |
2023-08-12 |
mouse |
| Huali Chen, Xue Wang, Mingming Tong, Dan Wu, Sisi Wu, Jiaxiang Chen, Xiaoxiao Wang, Xulei Wang, Yu Kang, Hong Tang, Chaoshu Tang, Wei Jian. Intermedin suppresses pressure overload cardiac hypertrophy through activation of autophagy. PloS one. vol 8. issue 5. 2013-11-25. PMID:23737997. |
we further observed that imd induced strong autophagy in hypertrophic hearts and cultured cells, which was paralleling with the decrease in cardiomyocyte size and apoptosis. |
2013-11-25 |
2023-08-12 |
mouse |
| Huali Chen, Xue Wang, Mingming Tong, Dan Wu, Sisi Wu, Jiaxiang Chen, Xiaoxiao Wang, Xulei Wang, Yu Kang, Hong Tang, Chaoshu Tang, Wei Jian. Intermedin suppresses pressure overload cardiac hypertrophy through activation of autophagy. PloS one. vol 8. issue 5. 2013-11-25. PMID:23737997. |
furthermore, an autophagy inhibitor, 3-ma, was used to block the imd-augmented autophagy level, and then the protection of imd on cardiomyocyte hypertrophy and apoptosis was almost abrogated. |
2013-11-25 |
2023-08-12 |
mouse |
| Huali Chen, Xue Wang, Mingming Tong, Dan Wu, Sisi Wu, Jiaxiang Chen, Xiaoxiao Wang, Xulei Wang, Yu Kang, Hong Tang, Chaoshu Tang, Wei Jian. Intermedin suppresses pressure overload cardiac hypertrophy through activation of autophagy. PloS one. vol 8. issue 5. 2013-11-25. PMID:23737997. |
these results indicate that the endogenous imd and its receptor complexes are induced in hypertrophic cardiomyocytes and proposed to play an important role in the pathogenesis of cardiac hypertrophy, and the autophagy stirred by imd supplementation is involved in its protection against cardiomyocyte hypertrophy and apoptosis through the activation of both camp/pka and mapk/erk1/2 pathways. |
2013-11-25 |
2023-08-12 |
mouse |
| Anna Foryst-Ludwig, Ulrich Kintsche. Sex differences in exercise-induced cardiac hypertrophy. Pflugers Archiv : European journal of physiology. vol 465. issue 5. 2013-11-14. PMID:23417601. |
in contrast to pathological forms of cardiac hypertrophy, exercise-induced increase of left ventricular mass is related to cardiac myocytes enlargement, with no apparent sign of fibrosis or apoptosis, and does usually not result in cardiac failure. |
2013-11-14 |
2023-08-12 |
human |
| Karina Huynh, Helen Kiriazis, Xiao-Jun Du, Jane E Love, Stephen P Gray, Karin A Jandeleit-Dahm, Julie R McMullen, Rebecca H Ritchi. Targeting the upregulation of reactive oxygen species subsequent to hyperglycemia prevents type 1 diabetic cardiomyopathy in mice. Free radical biology & medicine. vol 60. 2013-11-01. PMID:23454064. |
coenzyme q10 substantially limited type 1 diabetes-induced impairments in lv diastolic function (e:a ratio and deceleration time by echocardiography, lv end-diastolic pressure, and lv -dp/dt by micromanometry), lv remodeling (cardiomyocyte hypertrophy, cardiac fibrosis, apoptosis), and lv expression of proinflammatory mediators (tumor necrosis factor-α, with a similar trend for interleukin il-1β). |
2013-11-01 |
2023-08-12 |
mouse |
| Tamara Tajsic, Nicholas W Morrel. Smooth muscle cell hypertrophy, proliferation, migration and apoptosis in pulmonary hypertension. Comprehensive Physiology. vol 1. issue 1. 2013-10-30. PMID:23737174. |
smooth muscle cell hypertrophy, proliferation, migration and apoptosis in pulmonary hypertension. |
2013-10-30 |
2023-08-12 |
Not clear |
| Tamara Tajsic, Nicholas W Morrel. Smooth muscle cell hypertrophy, proliferation, migration and apoptosis in pulmonary hypertension. Comprehensive Physiology. vol 1. issue 1. 2013-10-30. PMID:23737174. |
underlying or contributing to the development of these lesions is hypertrophy, proliferation, migration, and resistance to apoptosis of medial cells and this article is concerned with the cellular and molecular mechanisms of these processes. |
2013-10-30 |
2023-08-12 |
Not clear |
| Tamara Tajsic, Nicholas W Morrel. Smooth muscle cell hypertrophy, proliferation, migration and apoptosis in pulmonary hypertension. Comprehensive Physiology. vol 1. issue 1. 2013-10-30. PMID:23737174. |
in the first part of the article we focus on the concept of smooth muscle cell phenotype and the difficulties surrounding the identification and characterization of the cell/cells involved in the remodelling of the vessel media and we review the general mechanisms of cell hypertrophy, proliferation, migration and apoptosis. |
2013-10-30 |
2023-08-12 |
Not clear |
| Laura J Janke, Chengcheng Liu, Peter Vogel, Jitesh Kawedia, Kelli L Boyd, Amy J Funk, Mary V Rellin. Primary epiphyseal arteriopathy in a mouse model of steroid-induced osteonecrosis. The American journal of pathology. vol 183. issue 1. 2013-10-24. PMID:23673001. |
proposed inciting mechanisms include intravascular thrombotic occlusion, marrow fat hypertrophy, osteocyte and/or endothelial cell apoptosis, hypercoagulability, and vasoconstriction of specific arteries and arterioles supplying bone. |
2013-10-24 |
2023-08-12 |
mouse |
| Rui Sheng, Zhen-Lun Gu, Mei-Lin Xi. Epigallocatechin gallate, the major component of polyphenols in green tea, inhibits telomere attrition mediated cardiomyocyte apoptosis in cardiac hypertrophy. International journal of cardiology. vol 162. issue 3. 2013-10-22. PMID:22000973. |
epigallocatechin gallate, the major component of polyphenols in green tea, inhibits telomere attrition mediated cardiomyocyte apoptosis in cardiac hypertrophy. |
2013-10-22 |
2023-08-12 |
Not clear |
| Atsuko Nakatsuka, Jun Wada, Hirofumi Makin. Cell cycle abnormality in metabolic syndrome and nuclear receptors as an emerging therapeutic target. Acta medica Okayama. vol 67. issue 3. 2013-10-22. PMID:23804135. |
in the accumulation of adipose tissues, cell cycle regulation is tightly linked to cellular processes such as proliferation, hypertrophy and apoptosis. |
2013-10-22 |
2023-08-12 |
Not clear |
| Iram Murtaza, Hong-Xia Wang, Sobia Mushtaq, Qamar Javed, Pei-Feng L. Interplay of Phosphorylated Apoptosis Repressor with CARD, Casein Kinase-2 and Reactive Oxygen Species in Regulating Endothelin-1-Induced Cardiomyocyte Hypertrophy. Iranian journal of basic medical sciences. vol 16. issue 8. 2013-10-09. PMID:24106598. |
interplay of phosphorylated apoptosis repressor with card, casein kinase-2 and reactive oxygen species in regulating endothelin-1-induced cardiomyocyte hypertrophy. |
2013-10-09 |
2023-08-12 |
Not clear |
| Iram Murtaza, Hong-Xia Wang, Sobia Mushtaq, Qamar Javed, Pei-Feng L. Interplay of Phosphorylated Apoptosis Repressor with CARD, Casein Kinase-2 and Reactive Oxygen Species in Regulating Endothelin-1-Induced Cardiomyocyte Hypertrophy. Iranian journal of basic medical sciences. vol 16. issue 8. 2013-10-09. PMID:24106598. |
the role of the apoptosis repressor with caspase recruitment domain (arc) in apoptosis and in certain hypertrophic responses has been previously investigated, but its regulation of endothelin-1 induced cardiac hypertrophy remains unknown. |
2013-10-09 |
2023-08-12 |
Not clear |
| Yasumoto Matsui, Atsushi Harad. [Aging of joint]. Clinical calcium. vol 23. issue 1. 2013-09-25. PMID:23268297. |
in oa cartilage, increased degradation and decreased production of major matrix components, like type ii collagen and aggrecan occur, as well as chondrocyte hypertrophy or apoptosis. |
2013-09-25 |
2023-08-12 |
Not clear |