| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Linn Moore, Dong Fan, Ratnadeep Basu, Vijay Kandalam, Zamaneh Kassir. Tissue inhibitor of metalloproteinases (TIMPs) in heart failure. Heart failure reviews. vol 17. issue 4-5. 2013-05-07. PMID:21717224. |
hence, disruption of the ecm will result in structural instability as well as activation of a number of signaling pathways that could lead to fibrosis, hypertrophy, and apoptosis. |
2013-05-07 |
2023-08-12 |
Not clear |
| Mohammad T Elnakish, Mohamed D H Hassona, Mazin A Alhaj, Leni Moldovan, Paul M L Janssen, Mahmood Khan, Hamdy H Hassanai. Rac-induced left ventricular dilation in thyroxin-treated ZmRacD transgenic mice: role of cardiomyocyte apoptosis and myocardial fibrosis. PloS one. vol 7. issue 8. 2013-04-25. PMID:22936985. |
moreover, rac-mediated o(2)·(-) generation, cardiomyocyte apoptosis, and myocardial fibrosis seem to play a pivotal role in the transition from cardiac hypertrophy to cardiac dilation and failure. |
2013-04-25 |
2023-08-12 |
mouse |
| Dominic P Del Re, Yanfei Yang, Noritsugu Nakano, Jaeyeaon Cho, Peiyong Zhai, Takanobu Yamamoto, Nailing Zhang, Norikazu Yabuta, Hiroshi Nojima, Duojia Pan, Junichi Sadoshim. Yes-associated protein isoform 1 (Yap1) promotes cardiomyocyte survival and growth to protect against myocardial ischemic injury. The Journal of biological chemistry. vol 288. issue 6. 2013-04-19. PMID:23275380. |
after chronic mi (28 days), yap(+/f)cre mice had significantly increased myocyte apoptosis and fibrosis, with attenuated compensatory cardiomyocyte hypertrophy, and further impaired function versus yap(+/f) control mice. |
2013-04-19 |
2023-08-12 |
mouse |
| Dominic P Del Re, Yanfei Yang, Noritsugu Nakano, Jaeyeaon Cho, Peiyong Zhai, Takanobu Yamamoto, Nailing Zhang, Norikazu Yabuta, Hiroshi Nojima, Duojia Pan, Junichi Sadoshim. Yes-associated protein isoform 1 (Yap1) promotes cardiomyocyte survival and growth to protect against myocardial ischemic injury. The Journal of biological chemistry. vol 288. issue 6. 2013-04-19. PMID:23275380. |
studies in isolated cardiomyocytes demonstrated that yap1 expression is sufficient to promote increased cell size and hypertrophic gene expression and protected cardiomyocytes against h(2)o(2)-induced cell death, whereas yap1 depletion attenuated phenylephrine-induced hypertrophy and augmented apoptosis. |
2013-04-19 |
2023-08-12 |
mouse |
| Eduardo Martinez-Abundis, Venkatesh Rajapurohitam, James V Haist, Xiaohong T Gan, Morris Karmazy. The obesity-related peptide leptin sensitizes cardiac mitochondria to calcium-induced permeability transition pore opening and apoptosis. PloS one. vol 7. issue 7. 2013-04-09. PMID:22848545. |
these effects were associated with increased apoptosis as evidenced by increased tunel staining and caspase 3 activity, both of which were prevented by the transition pore inhibitor sanglifehrin a. leptin enhanced stat3 activation whereas a stat 3 inhibitor peptide prevented leptin-induced mitochondrial transition pore opening as well as the hypertrophic and pro-apoptotic effects of the peptide. |
2013-04-09 |
2023-08-12 |
rat |
| Inês Falcão-Pires, Adelino F Leite-Moreir. Diabetic cardiomyopathy: understanding the molecular and cellular basis to progress in diagnosis and treatment. Heart failure reviews. vol 17. issue 3. 2013-04-05. PMID:21626163. |
left ventricular hypertrophy, metabolic abnormalities, extracellular matrix changes, small vessel disease, cardiac autonomic neuropathy, insulin resistance, oxidative stress, and apoptosis are the most important contributors to diabetic cardiomyopathy onset and progression. |
2013-04-05 |
2023-08-12 |
human |
| Bo Sun, Rong Huo, Yue Sheng, Yue Li, Xin Xie, Chang Chen, Hui-Bin Liu, Na Li, Cheng-Bo Li, Wen-Ting Guo, Jiu-Xin Zhu, Bao-Feng Yang, De-Li Don. Bone morphogenetic protein-4 mediates cardiac hypertrophy, apoptosis, and fibrosis in experimentally pathological cardiac hypertrophy. Hypertension (Dallas, Tex. : 1979). vol 61. issue 2. 2013-03-20. PMID:23248151. |
bone morphogenetic protein-4 mediates cardiac hypertrophy, apoptosis, and fibrosis in experimentally pathological cardiac hypertrophy. |
2013-03-20 |
2023-08-12 |
mouse |
| Bo Sun, Rong Huo, Yue Sheng, Yue Li, Xin Xie, Chang Chen, Hui-Bin Liu, Na Li, Cheng-Bo Li, Wen-Ting Guo, Jiu-Xin Zhu, Bao-Feng Yang, De-Li Don. Bone morphogenetic protein-4 mediates cardiac hypertrophy, apoptosis, and fibrosis in experimentally pathological cardiac hypertrophy. Hypertension (Dallas, Tex. : 1979). vol 61. issue 2. 2013-03-20. PMID:23248151. |
in this study, we investigated the role of bmp4 in cardiac hypertrophy, apoptosis, and fibrosis in experimentally pathological cardiac hypertrophy. |
2013-03-20 |
2023-08-12 |
mouse |
| Bo Sun, Rong Huo, Yue Sheng, Yue Li, Xin Xie, Chang Chen, Hui-Bin Liu, Na Li, Cheng-Bo Li, Wen-Ting Guo, Jiu-Xin Zhu, Bao-Feng Yang, De-Li Don. Bone morphogenetic protein-4 mediates cardiac hypertrophy, apoptosis, and fibrosis in experimentally pathological cardiac hypertrophy. Hypertension (Dallas, Tex. : 1979). vol 61. issue 2. 2013-03-20. PMID:23248151. |
in turn, bmp4 induced cardiomyocyte hypertrophy, apoptosis, and cardiac fibrosis, and these pathological consequences were inhibited by the treatment with bmp4 inhibitors noggin and dmh1. |
2013-03-20 |
2023-08-12 |
mouse |
| Bo Sun, Rong Huo, Yue Sheng, Yue Li, Xin Xie, Chang Chen, Hui-Bin Liu, Na Li, Cheng-Bo Li, Wen-Ting Guo, Jiu-Xin Zhu, Bao-Feng Yang, De-Li Don. Bone morphogenetic protein-4 mediates cardiac hypertrophy, apoptosis, and fibrosis in experimentally pathological cardiac hypertrophy. Hypertension (Dallas, Tex. : 1979). vol 61. issue 2. 2013-03-20. PMID:23248151. |
the underlying mechanism that bmp4-induced cardiomyocyte hypertrophy and apoptosis was through increasing nadph oxidase 4 expression and reactive oxygen species-dependent pathways. |
2013-03-20 |
2023-08-12 |
mouse |
| Bo Sun, Rong Huo, Yue Sheng, Yue Li, Xin Xie, Chang Chen, Hui-Bin Liu, Na Li, Cheng-Bo Li, Wen-Ting Guo, Jiu-Xin Zhu, Bao-Feng Yang, De-Li Don. Bone morphogenetic protein-4 mediates cardiac hypertrophy, apoptosis, and fibrosis in experimentally pathological cardiac hypertrophy. Hypertension (Dallas, Tex. : 1979). vol 61. issue 2. 2013-03-20. PMID:23248151. |
lentivirus-mediated overexpression of bmp4 recapitulated hypertrophy and apoptosis in cultured cardiomyocytes. |
2013-03-20 |
2023-08-12 |
mouse |
| Mei Zhao, Wei-Jin Zan. [The bidirectional roles of macroautophagy in the regulation of heart disease]. Sheng li ke xue jin zhan [Progress in physiology]. vol 42. issue 2. 2013-03-14. PMID:21770252. |
this paper reviews the research progress of macroautophagy in the regulation of heart disease, including macroautophagy formation, the relationship between macroautophagy and apoptosis, macroautophagy under the conditions of myocardial ischemia-reperfusion, hypertrophy and heart failure, in order to find a new method for the treatment. |
2013-03-14 |
2023-08-12 |
Not clear |
| Giuseppe Distefano, Pietro Sciacc. Molecular pathogenesis of myocardial remodeling and new potential therapeutic targets in chronic heart failure. Italian journal of pediatrics. vol 38. 2013-03-12. PMID:22971785. |
typical features of myocardial remodeling are represented by cardiomyocytes hypertrophy and apoptosis, extracellular matrix alterations, mesenchymal fibrotic and phlogistic processes and by cardiac gene expression modifications with fetal genetic program reactivation. |
2013-03-12 |
2023-08-12 |
Not clear |
| Yuzhi Ge, Shujuan Pan, Di Guan, Hong Yin, Yong Fan, Jingjing Liu, Shuhua Zhang, Hongjie Zhang, Lili Feng, Yunxia Wang, Ruxiang Xu, James Q Yi. MicroRNA-350 induces pathological heart hypertrophy by repressing both p38 and JNK pathways. Biochimica et biophysica acta. vol 1832. issue 1. 2013-03-04. PMID:23000971. |
here we report that mir-350 plays a key role in determining pathological cardiomyocyte hypertrophy and apoptosis. |
2013-03-04 |
2023-08-12 |
rat |
| Yuzhi Ge, Shujuan Pan, Di Guan, Hong Yin, Yong Fan, Jingjing Liu, Shuhua Zhang, Hongjie Zhang, Lili Feng, Yunxia Wang, Ruxiang Xu, James Q Yi. MicroRNA-350 induces pathological heart hypertrophy by repressing both p38 and JNK pathways. Biochimica et biophysica acta. vol 1832. issue 1. 2013-03-04. PMID:23000971. |
our data provide the first evidence that mir-350 is a critical regulator of pathological cardiac hypertrophy and apoptosis in rats. |
2013-03-04 |
2023-08-12 |
rat |
| Megan Whitnall, Yohan Suryo Rahmanto, Michael L-H Huang, Federica Saletta, Hiu Chuen Lok, Lucía Gutiérrez, Francisco J Lázaro, Adam J Fleming, Tim G St Pierre, Marc R Mikhael, Prem Ponka, Des R Richardso. Identification of nonferritin mitochondrial iron deposits in a mouse model of Friedreich ataxia. Proceedings of the National Academy of Sciences of the United States of America. vol 109. issue 50. 2013-02-28. PMID:23169664. |
considering fe deficiency can induce apoptosis and cell death, we examined the effect of dietary fe supplementation, which led to body fe loading and limited the cardiac hypertrophy in mck mutants. |
2013-02-28 |
2023-08-12 |
mouse |
| Dirk Westermann, Peter Moritz Becher, Diana Lindner, Kostantinos Savvatis, Yu Xia, Matthias Fröhlich, Sebastian Hoffmann, Heinz-Peter Schultheiss, Carsten Tschöp. Selective PDE5A inhibition with sildenafil rescues left ventricular dysfunction, inflammatory immune response and cardiac remodeling in angiotensin II-induced heart failure in vivo. Basic research in cardiology. vol 107. issue 6. 2013-02-13. PMID:23117837. |
c57bl6/j mice were subjected to angii-induced cardiac hypertrophy for 3 weeks and cardiac dysfunction, cardiac inflammatory stress response, adverse remodeling as well as apoptosis were documented. |
2013-02-13 |
2023-08-12 |
mouse |
| Dirk Westermann, Peter Moritz Becher, Diana Lindner, Kostantinos Savvatis, Yu Xia, Matthias Fröhlich, Sebastian Hoffmann, Heinz-Peter Schultheiss, Carsten Tschöp. Selective PDE5A inhibition with sildenafil rescues left ventricular dysfunction, inflammatory immune response and cardiac remodeling in angiotensin II-induced heart failure in vivo. Basic research in cardiology. vol 107. issue 6. 2013-02-13. PMID:23117837. |
this effect was associated with less lv hypertrophy, remodeling, cardiac inflammation and apoptosis. |
2013-02-13 |
2023-08-12 |
mouse |
| Dariush Honardoust, Jie Ding, Mathew Varkey, Heather A Shankowsky, Edward E Tredge. Deep dermal fibroblasts refractory to migration and decorin-induced apoptosis contribute to hypertrophic scarring. Journal of burn care & research : official publication of the American Burn Association. vol 33. issue 5. 2013-02-04. PMID:22210076. |
deep dermal fibroblasts refractory to migration and decorin-induced apoptosis contribute to hypertrophic scarring. |
2013-02-04 |
2023-08-12 |
Not clear |
| Hong Zhang, Yan Zhang, Yi-Ping Jiang, Lan-Ke Zhang, Cheng Peng, Kun He, Khalid Rahman, Lu-Ping Qi. Curative effects of oleanolic Acid on formed hypertrophic scars in the rabbit ear model. Evidence-based complementary and alternative medicine : eCAM. vol 2012. 2013-01-18. PMID:23326292. |
these results suggest that oa has the favorable curative effects on formed hypertrophic scars in the rabbit ear model, and the possible mechanism of action is that oa decreases hsfs proliferation and increases hsfs apoptosis by reduction of p311 gene expression and tgf-β(1) production, inhibition of timp-1 secretion, enhancement of mmp-2 activity, and subsequently facilitation of degradation of collagen types i and iii. |
2013-01-18 |
2023-08-12 |
rabbit |