| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Asmaa Mohammed ShamsEldeen, Hend Ashour, Heba Samy Shoukry, Mostafa Fadel, Samaa Samir Kamar, Marwan Aabdelbaset, Laila Ahmed Rashed, Hania Ibrahim Amma. Combined treatment with systemic resveratrol and resveratrol preconditioned mesenchymal stem cells, maximizes antifibrotic action in diabetic cardiomyopathy. Journal of cellular physiology. vol 234. issue 7. 2020-05-20. PMID:30537190. |
dm group revealed significant myocardial hypertrophy, apoptosis, interstitial fibrosis, and microvascular affection. |
2020-05-20 |
2023-08-13 |
rat |
| Yinglu Ren, Xiangyang Chen, Peng Li, Huimin Zhang, Congping Su, Zifan Zeng, Yan Wu, Xuan Xie, Qing Wang, Jing Han, Shuzhen Guo, Bin Liu, Wei Wan. Si-Miao-Yong-An decoction ameliorates cardiac function through restoring the equilibrium of SOD and NOX2 in heart failure mice. Pharmacological research. vol 146. 2020-05-11. PMID:31228552. |
smyad treatment significantly ameliorated cardiac function, reduced collagen deposition and cardiomyocyte apoptosis, reversed cardiac hypertrophy and down-regulated the expression levels of anp and bnp mrna compared with those in hf mice. |
2020-05-11 |
2023-08-13 |
mouse |
| Santanu Rana, Ritwik Datta, Ratul Datta Chaudhuri, Emeli Chatterjee, Mamta Chawla-Sarkar, Sagartirtha Sarka. Nanotized PPARα Overexpression Targeted to Hypertrophied Myocardium Improves Cardiac Function by Attenuating the p53-GSK3β-Mediated Mitochondrial Death Pathway. Antioxidants & redox signaling. vol 30. issue 5. 2020-05-04. PMID:29631413. |
in the present study, consequences of pparα augmentation were evaluated for amelioration of chronic oxidative stress, myocyte apoptosis, and cardiac function during pathological cardiac hypertrophy. |
2020-05-04 |
2023-08-13 |
Not clear |
| Yongxia Cheng, Jingchao Li, Chong Wang, Heran Yang, Ying Wang, Tao Zhan, Sufen Guo, Jun Liang, Yuxin Bai, Jianbo Yu, Guibo Li. Inhibition of long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 attenuates high glucose-induced cardiomyocyte apoptosis via regulation of miR-181a-5p. Experimental animals. vol 69. issue 1. 2020-04-20. PMID:31353329. |
in this study, we established a mouse dcm model via streptozocin injection as evidenced by cell hypertrophy and cell apoptosis of myocardial tissue, and found that malat1 expression was upregulated in the myocardium in dcm mice. |
2020-04-20 |
2023-08-13 |
mouse |
| Zhengbo Zhao, Han Liu, Yu Li, Jingxiu Tian, Songbai Den. Wnt-C59 Attenuates Pressure Overload-Induced Cardiac Hypertrophy via Interruption of Wnt Pathway. Medical science monitor : international medical journal of experimental and clinical research. vol 26. 2020-04-15. PMID:32279067. |
histologically, wnt-c59 attenuated tac-induced increase in heart mass, cross-section area of cardiomyocyte, cardiac fibrosis, cardiomyocyte apoptosis, and expression of the hypertrophic biomarkers ß-mhc, anp, and bnp. |
2020-04-15 |
2023-08-13 |
mouse |
| Zhengbo Zhao, Han Liu, Dongmei Gu. Aliskiren attenuates cardiac dysfunction by modulation of the mTOR and apoptosis pathways. Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas. vol 53. issue 2. 2020-04-07. PMID:31994601. |
the aim of the present study was to investigate the role of als in mammalian target of rapamycin (mtor) and apoptosis signaling using in vivo and in vitro models of cardiac hypertrophy. |
2020-04-07 |
2023-08-13 |
rat |
| Zhengbo Zhao, Han Liu, Dongmei Gu. Aliskiren attenuates cardiac dysfunction by modulation of the mTOR and apoptosis pathways. Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas. vol 53. issue 2. 2020-04-07. PMID:31994601. |
furthermore, ang ii triggered the activation of the mtor and apoptosis pathways in hypertrophic cardiomyocytes that were inhibited by als treatment. |
2020-04-07 |
2023-08-13 |
rat |
| Zhengbo Zhao, Han Liu, Dongmei Gu. Aliskiren attenuates cardiac dysfunction by modulation of the mTOR and apoptosis pathways. Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas. vol 53. issue 2. 2020-04-07. PMID:31994601. |
these results indicated that als alleviated cardiac hypertrophy through inhibition of the mtor and apoptosis pathways in cardiomyocytes. |
2020-04-07 |
2023-08-13 |
rat |
| Que Wang, Xiaoxue Yu, Lin Dou, Xiuqing Huang, Kaiyi Zhu, Jun Guo, Mingjing Yan, Siming Wang, Yong Man, Weiqing Tang, Tao Shen, Jian L. miR-154-5p Functions as an Important Regulator of Angiotensin II-Mediated Heart Remodeling. Oxidative medicine and cellular longevity. vol 2019. 2020-04-02. PMID:31612078. |
second, overexpression of mir-154-5p to a level similar to that induced by angii was sufficient to trigger cardiomyocyte hypertrophy and apoptosis, which is associated with profound activation of oxidative stress and inflammation. |
2020-04-02 |
2023-08-13 |
mouse |
| Que Wang, Xiaoxue Yu, Lin Dou, Xiuqing Huang, Kaiyi Zhu, Jun Guo, Mingjing Yan, Siming Wang, Yong Man, Weiqing Tang, Tao Shen, Jian L. miR-154-5p Functions as an Important Regulator of Angiotensin II-Mediated Heart Remodeling. Oxidative medicine and cellular longevity. vol 2019. 2020-04-02. PMID:31612078. |
third, mir-154-5p directly inhibited arylsulfatase b (arsb) expression by interacting with its 3'-utr and promoted cardiomyocyte hypertrophy and apoptosis. |
2020-04-02 |
2023-08-13 |
mouse |
| Que Wang, Xiaoxue Yu, Lin Dou, Xiuqing Huang, Kaiyi Zhu, Jun Guo, Mingjing Yan, Siming Wang, Yong Man, Weiqing Tang, Tao Shen, Jian L. miR-154-5p Functions as an Important Regulator of Angiotensin II-Mediated Heart Remodeling. Oxidative medicine and cellular longevity. vol 2019. 2020-04-02. PMID:31612078. |
lastly, the angiotensin type 1 receptor blocker telmisartan attenuated angii-induced cardiac hypertrophy, apoptosis, and fibrosis by blocking the increase in mir-154-5p expression. |
2020-04-02 |
2023-08-13 |
mouse |
| Que Wang, Xiaoxue Yu, Lin Dou, Xiuqing Huang, Kaiyi Zhu, Jun Guo, Mingjing Yan, Siming Wang, Yong Man, Weiqing Tang, Tao Shen, Jian L. miR-154-5p Functions as an Important Regulator of Angiotensin II-Mediated Heart Remodeling. Oxidative medicine and cellular longevity. vol 2019. 2020-04-02. PMID:31612078. |
based on these results, increased cardiac mir-154-5p expression is both necessary and sufficient for angii-induced cardiomyocyte hypertrophy and apoptosis, suggesting that the upregulation of mir-154-5p may be a crucial pathological factor and a potential therapeutic target for cardiac remodeling. |
2020-04-02 |
2023-08-13 |
mouse |
| Kai-Chun Cheng, Yingxiao Li, Wei-Ting Chang, Zhih-Cherng Chen, Juei-Tang Cheng, Cheng-Chia Tsa. Ubiquitin-protein ligase E3a (UBE3A) as a new biomarker of cardiac hypertrophy in cell models. Journal of food and drug analysis. vol 27. issue 1. 2020-03-23. PMID:30648591. |
the pathophysiology of hypertrophy is complex and multifactorial, a series of molecular and cellular changes are participated, such as activation of different signaling pathways, a switch of fetal gene program in the myocardium, and apoptosis. |
2020-03-23 |
2023-08-13 |
Not clear |
| Qinghai Meng, Yao Guo, Dini Zhang, Qichun Zhang, Yu Li, Huimin Bia. Tongsaimai reverses the hypertension and left ventricular remolding caused by abdominal aortic constriction in rats. Journal of ethnopharmacology. vol 246. 2020-03-23. PMID:31415848. |
moreover, tsm alleviated cardiac histomorphology injury resulting from aac, including reducing cardiomyocyte hypertrophy, fibrous connective tissue hyperplasia, cardiomyocyte apoptosis, replacement fibrosis and the disorders of myocardial myofibrils, intercalated discs, mitochondria and mitochondrial crista. |
2020-03-23 |
2023-08-13 |
rat |
| Juan Jin, Jianguang Gong, Li Zhao, Hongjuan Zhang, Qiang He, Xinxin Jian. Inhibition of high mobility group box 1 (HMGB1) attenuates podocyte apoptosis and epithelial-mesenchymal transition by regulating autophagy flux. Journal of diabetes. vol 11. issue 10. 2020-03-12. PMID:30864227. |
podocyte injury, characterized by podocyte hypertrophy, apoptosis, and epithelial-mesenchymal transition (emt), is the major causative factor of diabetic nephropathy (dn). |
2020-03-12 |
2023-08-13 |
Not clear |
| Thomas Senoner, Wolfgang Dicht. Oxidative Stress in Cardiovascular Diseases: Still a Therapeutic Target? Nutrients. vol 11. issue 9. 2020-03-05. PMID:31487802. |
ros also negatively influence myocardial calcium handling, causing arrhythmia, and augment cardiac remodeling by inducing hypertrophic signaling and apoptosis. |
2020-03-05 |
2023-08-13 |
Not clear |
| Zhenzhen Lu, Yifei Zhong, Wangyi Liu, Ling Xiang, Yueyi Den. The Efficacy and Mechanism of Chinese Herbal Medicine on Diabetic Kidney Disease. Journal of diabetes research. vol 2019. 2020-02-27. PMID:31534972. |
the pathological features of dkd are the hypertrophy of mesangial cells, apoptosis of podocytes, glomerular basement membrane (gbm) thickening, accumulation of extracellular matrix (ecm), glomerular sclerosis, and tubulointerstitial fibrosis. |
2020-02-27 |
2023-08-13 |
Not clear |
| Marco Cassano, Stefano Biressi, Amanda Finan, Laura Benedetti, Claudia Omes, Renata Boratto, Frank Martin, Marcello Allegretti, Vania Broccoli, Gabriella Cusella De Angelis, Paolo M Comoglio, Cristina Basilico, Yvan Torrente, Paolo Michieli, Giulio Cossu, Maurilio Sampaoles. Correction: Magic-Factor 1, a Partial Agonist of Met, Induces Muscle Hypertrophy by Protecting Myogenic Progenitors from Apoptosis. PloS one. vol 14. issue 7. 2020-02-25. PMID:31339946. |
correction: magic-factor 1, a partial agonist of met, induces muscle hypertrophy by protecting myogenic progenitors from apoptosis. |
2020-02-25 |
2023-08-13 |
Not clear |
| Junqin Sheng, Hongyan Li, Qin Dai, Chang Lu, Min Xu, Jisheng Zhang, Jianxun Fen. DUSP1 recuses diabetic nephropathy via repressing JNK-Mff-mitochondrial fission pathways. Journal of cellular physiology. vol 234. issue 3. 2020-01-20. PMID:30191967. |
lower dusp1 expression was associated with glucose metabolism disorder, renal dysfunction, kidney hypertrophy, renal fibrosis, and glomerular apoptosis. |
2020-01-20 |
2023-08-13 |
Not clear |
| Aiko Ito, Yoshiki Ohnuki, Kenji Suita, Misao Ishikawa, Yasumasa Mototani, Kouichi Shiozawa, Naoya Kawamura, Yuka Yagisawa, Megumi Nariyama, Daisuke Umeki, Yoshiki Nakamura, Satoshi Okumur. Role of β-adrenergic signaling in masseter muscle. PloS one. vol 14. issue 4. 2020-01-07. PMID:30986276. |
in cardiac muscle, chronic β1-ar stimulation induced cardiac hypertrophy, fibrosis and myocyte apoptosis, whereas chronic β2-ar stimulation induced cardiac hypertrophy without histological abnormalities. |
2020-01-07 |
2023-08-13 |
mouse |