All Relations between apoptosis and hypertrophic

Publication Sentence Publish Date Extraction Date Species
Rashmi Choudhary, K P Mishra, C Subramanya. Prevention of isoproterenol-induced cardiac hypertrophy by eugenol, an antioxidant. Indian journal of clinical biochemistry : IJCB. vol 21. issue 2. 2012-10-30. PMID:23105625. intraperitoneal administration of isoproterenol (1 mg/kg body wt/day for 10 days) induced cardiac hypertrophy with increased heart weight and enhanced apoptosis of myocytes concomitant with accumulation of reactive oxygen species, decreased glutathione contents, increased activities of calcineurin and protein kinase c in ventricular tissue. 2012-10-30 2023-08-12 rat
Ming Ding, Yaojuan Lu, Sam Abbassi, Feifei Li, Xin Li, Yu Song, Valérie Geoffroy, Hee-Jeong Im, Qiping Zhen. Targeting Runx2 expression in hypertrophic chondrocytes impairs endochondral ossification during early skeletal development. Journal of cellular physiology. vol 227. issue 10. 2012-10-29. PMID:22223437. histological analysis showed elongated hypertrophic zones in transgenic mice, with less von kossa and tunel staining in long bone sections at both e17.5 and p1 stages, suggesting defective mineralization due to delayed chondrocyte maturation or apoptosis. 2012-10-29 2023-08-12 mouse
Salil Sharma, Jing Liu, Jianqin Wei, Huijun Yuan, Taifang Zhang, Nanette H Bishopri. Repression of miR-142 by p300 and MAPK is required for survival signalling via gp130 during adaptive hypertrophy. EMBO molecular medicine. vol 4. issue 7. 2012-10-24. PMID:22367739. forced expression of mir-142 during hypertrophic growth induced extensive apoptosis and cardiac dysfunction; conversely, loss of mir-142 fully rescued cardiac function in a murine heart failure model. 2012-10-24 2023-08-12 human
Sheng-jiang Guan, Zhi-hong Ma, Yan-ling Wu, Jian-ping Zhang, Feng Liang, J Woodrow Weiss, Qian-yu Guo, Jiang-yan Wang, En-sheng Ji, Li Ch. Long-term administration of fasudil improves cardiomyopathy in streptozotocin-induced diabetic rats. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association. vol 50. issue 6. 2012-10-09. PMID:22429817. these effects could be attributed to regulation of antioxidative activities, suppression of myocardial hypertrophy, apoptosis, fibrosis and subsequent cardiac remodeling. 2012-10-09 2023-08-12 rat
T Ueland, P Aukrust, J K Damas, L Gullestad, A Yndesta. The tumor necrosis factor superfamily in heart failure. Future cardiology. vol 2. issue 1. 2012-10-02. PMID:19804137. all ligands in the tnf superfamily have the potential to activate nf-kappab, leading to transcription of genes involved in apoptosis, cell survival, proliferation, inflammation and hypertrophic signaling in cardiomyocytes. 2012-10-02 2023-08-12 human
Lars Gullestad, Thor Ueland, Leif Erik Vinge, Alexandra Finsen, Arne Yndestad, Pål Aukrus. Inflammatory cytokines in heart failure: mediators and markers. Cardiology. vol 122. issue 1. 2012-10-02. PMID:22699305. there is strong evidence that these mediators are involved in processes leading to cardiac remodeling such as hypertrophy, fibrosis and apoptosis. 2012-10-02 2023-08-12 Not clear
Hai-Yi Yu, Yan-Hong Guo, Wei Ga. [Mitochondrial fusion protein Mfn2 and cardiovascular diseases]. Sheng li ke xue jin zhan [Progress in physiology]. vol 41. issue 1. 2012-10-01. PMID:21417008. mfn2 is a signaling molecule, plays an important role in cell proliferation, differentiation and apoptosis, which participates in the pathophysiology of several cardiovascular diseases, such as hypertension, restenosis after angioplasty, atherosclerosis, cardiac hypertrophy, and cardiac oxidative stress injury. 2012-10-01 2023-08-12 Not clear
Nicole Stieger, Kirstin Worthmann, Beina Teng, Stefan Engeli, Anibh M Das, Hermann Haller, Mario Schiffe. Impact of high glucose and transforming growth factor-β on bioenergetic profiles in podocytes. Metabolism: clinical and experimental. vol 61. issue 8. 2012-10-01. PMID:22365040. various factors in the diabetic milieu lead to serious podocyte stress driving the cells toward cell cycle arrest (p27(kip1)), hypertrophy, detachment, and apoptosis. 2012-10-01 2023-08-12 Not clear
Chris Tikellis, Raelene Pickering, Despina Tsorotes, Xiao-Jun Du, Helen Kiriazis, Thu-Phuc Nguyen-Huu, Geoffrey A Head, Mark E Cooper, Merlin C Thoma. Interaction of diabetes and ACE2 in the pathogenesis of cardiovascular disease in experimental diabetes. Clinical science (London, England : 1979). vol 123. issue 8. 2012-09-21. PMID:22616805. this was associated structurally with thinning of the lv (left ventricular) wall and mild ventricular dilatation, and histologically with increased cardiomyocyte apoptosis on tunel (terminal deoxynucleotidyl transferase-mediated dutp nick-end labelling) staining and compensatory hypertrophy denoted by an increased cardiomyocyte cross-sectional area. 2012-09-21 2023-08-12 mouse
Sushma Reddy, Mingming Zhao, Dong-Qing Hu, Giovanni Fajardo, Shijun Hu, Zhumur Ghosh, Viswanathan Rajagopalan, Joseph C Wu, Daniel Bernstei. Dynamic microRNA expression during the transition from right ventricular hypertrophy to failure. Physiological genomics. vol 44. issue 10. 2012-09-20. PMID:22454450. the transition from hypertrophy to heart failure is characterized by apoptosis and fibrosis (mirs-34, 21, 1). 2012-09-20 2023-08-12 Not clear
Brittany A Law, Scott P Levick, Wayne E Carve. Alterations in cardiac structure and function in a murine model of chronic alcohol consumption. Microscopy and microanalysis : the official journal of Microscopy Society of America, Microbeam Analysis Society, Microscopical Society of Canada. vol 18. issue 3. 2012-09-20. PMID:22571914. throughout the study, an increase in cardiomyocyte hypertrophy, cardiac fibrosis, apoptosis, tgf-β, and the presence of α-sma-positive cells were determined. 2012-09-20 2023-08-12 mouse
Caroline B Marshall, Ron D Krofft, Jeffrey W Pippin, Stuart J Shanklan. CDK inhibitor p21 is prosurvival in adriamycin-induced podocyte injury, in vitro and in vivo. American journal of physiology. Renal physiology. vol 298. issue 5. 2012-09-18. PMID:20130121. in response to injury, the highly specialized and terminally differentiated glomerular visceral epithelial cell, or podocyte, may undergo several cell fates, including dedifferentiation and proliferation, persistent cell cycle arrest, hypertrophy, apoptosis, or necrosis. 2012-09-18 2023-08-12 mouse
Anke J Tijsen, Yigal M Pinto, Esther E Creemer. Non-cardiomyocyte microRNAs in heart failure. Cardiovascular research. vol 93. issue 4. 2012-09-17. PMID:22180601. myocyte hypertrophy, cardiomyocyte apoptosis, interstitial fibrosis, reduced capillary density, and activation of the immune system are all involved in the pathogenesis and progression of heart failure (hf). 2012-09-17 2023-08-12 Not clear
Jong Hui Suh, Eunmi Choi, Min-Ji Cha, Byeong-Wook Song, Onju Ham, Se-Yeon Lee, Cheesoon Yoon, Chang-Yeon Lee, Jun-Hee Park, Sun Hee Lee, Ki-Chul Hwan. Up-regulation of miR-26a promotes apoptosis of hypoxic rat neonatal cardiomyocytes by repressing GSK-3β protein expression. Biochemical and biophysical research communications. vol 423. issue 2. 2012-09-17. PMID:22664106. the mirnas play important roles in regulating cardiac physiological and pathological events such as hypertrophy, apoptosis, and heart failure. 2012-09-17 2023-08-12 rat
Hwanhee Oh, Je-Hwang Ryu, Jimin Jeon, Siyoung Yang, Churl-Hong Chun, Hongryeol Park, Hyung Joon Kim, Woo-Shin Kim, Hong-Hee Kim, Young-Guen Kwon, Jang-Soo Chu. Misexpression of Dickkopf-1 in endothelial cells, but not in chondrocytes or hypertrophic chondrocytes, causes defects in endochondral ossification. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. vol 27. issue 6. 2012-09-13. PMID:22407773. the defects are caused by the inhibition of angiogenesis in developing bone and subsequent inhibition of apoptosis of hypertrophic chondrocytes and cartilage resorption. 2012-09-13 2023-08-12 mouse
You-mei Zuo, Xing-hui Wang, Shan Gao, Ye Zhan. Oligomerized grape seed proanthocyanidins ameliorates isoproterenol-induced cardiac remodeling in rats: role of oxidative stress. Phytotherapy research : PTR. vol 25. issue 5. 2012-09-12. PMID:21077263. the effects of oligomerized grape seed proanthocyanidins (gsp) on haemodynamics, cardiac hypertrophy and fibrosis as well as apoptosis signal-regulating kinase 1 (ask1) and nuclear factor-κb (nf-κb) cascades in isoproterenol (iso)-induced cardiac remodelling (cr) rat model were investigated, in addition, the serum sod activities and mda content were assayed. 2012-09-12 2023-08-12 rat
Hongyan Zhu, Guo-Chang Fa. Role of microRNAs in the reperfused myocardium towards post-infarct remodelling. Cardiovascular research. vol 94. issue 2. 2012-09-07. PMID:22038740. myocardial ischaemia/reperfusion (i/r)-induced remodelling generally includes cell death (necrosis and apoptosis), myocyte hypertrophy, angiogenesis, cardiac fibrosis, and myocardial dysfunction. 2012-09-07 2023-08-12 Not clear
Jack W Penn, Adriaan O Grobbelaar, Kerstin J Rolf. The role of the TGF-β family in wound healing, burns and scarring: a review. International journal of burns and trauma. vol 2. issue 1. 2012-08-30. PMID:22928164. other putative mechanisms which may underlie the pathogenesis of hypertrophic scars include excessive inflammation, excessive angiogenesis, altered levels of matrix metalloproteinases, growth factors, and delayed apoptosis of fibrotic myofibroblasts either due to p53 genetic alterations or tensile forces across the wound. 2012-08-30 2023-08-12 human
Rong-Tao Yang, Chi Zhang, Yong Liu, Hai-Hua Zhou, Zu-Bing L. Autophagy prior to chondrocyte cell death during the degeneration of Meckel's cartilage. Anatomical record (Hoboken, N.J. : 2007). vol 295. issue 5. 2012-08-27. PMID:22371349. terminal deoxynucleotidyltransferase-mediated dutp-biotin nick-end labeling assay and caspase 3 expression demonstrated that apoptosis was detected in the lateral part of terminal hypertrophic chondrocytes along the degeneration area of meckel's cartilage. 2012-08-27 2023-08-12 mouse
Mary B Goldrin. Chondrogenesis, chondrocyte differentiation, and articular cartilage metabolism in health and osteoarthritis. Therapeutic advances in musculoskeletal disease. vol 4. issue 4. 2012-08-23. PMID:22859926. following chondrogenesis, the chondrocytes remain as resting cells to form the articular cartilage or undergo proliferation, terminal differentiation to chondrocyte hypertrophy, and apoptosis in a process termed endochondral ossification, whereby the hypertrophic cartilage is replaced by bone. 2012-08-23 2023-08-12 mouse