| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Nathalia Fonseca Nadur, Luciana Luiz de Azevedo, Lucas Caruso, Cedric Stephan Graebin, Renata Barbosa Lacerda, Arthur Eugen Kümmerl. The long and winding road of designing phosphodiesterase inhibitors for the treatment of heart failure. European journal of medicinal chemistry. vol 212. 2021-04-23. PMID:33412421. |
cyclic nucleotide phosphodiesterases (pdes) are a superfamily of enzymes known to play a critical role in the indirect regulation of several intracellular metabolism pathways through the selective hydrolysis of the phosphodiester bonds of specific second messenger substrates such as camp (3',5'-cyclic adenosine monophosphate) and cgmp (3',5'-cyclic guanosine monophosphate), influencing the hypertrophy, contractility, apoptosis and fibroses in the cardiovascular system. |
2021-04-23 |
2023-08-13 |
Not clear |
| Jierong Luo, Dan Yan, Sisi Li, Shiming Liu, Fei Zeng, Chi Wai Cheung, Hong Liu, Michael G Irwin, Huansen Huang, Zhengyuan Xi. Allopurinol reduces oxidative stress and activates Nrf2/p62 to attenuate diabetic cardiomyopathy in rats. Journal of cellular and molecular medicine. vol 24. issue 2. 2021-04-22. PMID:31856386. |
in vitro, alp increased nrf2 and reduced the hyperglycaemia-induced increases of h9c2 cardiomyocyte hypertrophy, oxidative stress, apoptosis and autophagy, and enhanced cellular viability. |
2021-04-22 |
2023-08-13 |
rat |
| E Jozefczuk, T J Guzik, M Siedlinsk. Significance of sphingosine-1-phosphate in cardiovascular physiology and pathology. Pharmacological research. vol 156. 2021-04-22. PMID:32278039. |
moreover, s1p controls both acute cardiac responses (cardiac inotropy and chronotropy), as well as chronic processes (such as apoptosis and hypertrophy), hence numerous studies demonstrate significance of s1p in the pathogenesis of hypertrophic/fibrotic heart disease, myocardial infarction and heart failure. |
2021-04-22 |
2023-08-13 |
Not clear |
| Zhi-Yuan Wu, Hui-Jun Zhang, Zhi-Hong Zhou, Zhan-Peng Li, Si-Mu Liao, Ze-Yong Wu, Hai-Hua Huang, Yu-Cang Sh. The effect of inhibiting exosomes derived from adipose-derived stem cells via the TGF-β1/Smad pathway on the fibrosis of keloid fibroblasts. Gland surgery. vol 10. issue 3. 2021-04-13. PMID:33842249. |
this paper discusses the effect of adipose-derived stem cell exosomes (adscs-exo) on the proliferation and apoptosis of kfs and its possible mechanism, in order to provide reference for the clinical intervention of hypertrophic scar. |
2021-04-13 |
2023-08-13 |
Not clear |
| Wei Wang, Hao Zhen. Myocardial Infarction: The Protective Role of MiRNAs in Myocardium Pathology. Frontiers in cardiovascular medicine. vol 8. 2021-03-23. PMID:33748196. |
mi leads to myocardial apoptosis, cardiomyocyte fibrosis, and cardiomyocyte hypertrophy, ultimately leading to heart failure, and death. |
2021-03-23 |
2023-08-13 |
Not clear |
| Yanli Zhao, Qi Zheng, Hanchao Gao, Mengtao Cao, Huiyun Wang, Rong Chang, Changchun Zen. Celecoxib alleviates pathological cardiac hypertrophy and fibrosis via M1-like macrophage infiltration in neonatal mice. iScience. vol 24. issue 3. 2021-03-23. PMID:33748715. |
cyclooxygenase-2 (cox-2) overexpression results in inflammatory response, cardiac cell apoptosis, and hypertrophy in adult heart after injury. |
2021-03-23 |
2023-08-13 |
mouse |
| Dong Guo, Yuerong Xu, Jian Ding, Jiaying Dong, Ning Jia, Yan Li, Mingming Zhan. Roles and Clinical Applications of Exosomes in Cardiovascular Disease. BioMed research international. vol 2020. 2021-03-22. PMID:32596327. |
we here review recent insights gained into the role of exosomes in apoptosis, hypertrophy, angiogenesis, fibrosis, and inflammation in cvd pathophysiology and progression and the application and mechanisms of exosomes as therapeutic agents for cvd. |
2021-03-22 |
2023-08-13 |
Not clear |
| Jinsheng Lai, Chen Che. The Role of Epoxyeicosatrienoic Acids in Cardiac Remodeling. Frontiers in physiology. vol 12. 2021-03-16. PMID:33716791. |
in the following, the roles of eets in cardiac remodeling, with a particular emphasis on myocardial hypertrophy, apoptosis, fibrosis, inflammation, and angiogenesis, will be summarized. |
2021-03-16 |
2023-08-13 |
Not clear |
| Xiaoyan Li, Hue Thi Le, Fuyuki Sato, Tong Ho Kang, Makoto Makishima, Liangjun Zhong, Yi Liu, Lijia Guo, Ujjal K Bhawa. Dec1 deficiency protects the heart from fibrosis, inflammation, and myocardial cell apoptosis in a mouse model of cardiac hypertrophy. Biochemical and biophysical research communications. vol 532. issue 4. 2021-03-11. PMID:32896382. |
dec1 deficiency protects the heart from fibrosis, inflammation, and myocardial cell apoptosis in a mouse model of cardiac hypertrophy. |
2021-03-11 |
2023-08-13 |
mouse |
| Xiaoyan Li, Hue Thi Le, Fuyuki Sato, Tong Ho Kang, Makoto Makishima, Liangjun Zhong, Yi Liu, Lijia Guo, Ujjal K Bhawa. Dec1 deficiency protects the heart from fibrosis, inflammation, and myocardial cell apoptosis in a mouse model of cardiac hypertrophy. Biochemical and biophysical research communications. vol 532. issue 4. 2021-03-11. PMID:32896382. |
this study explored the effects of dec1 on cardiac fibrosis, inflammation, and apoptosis in hypertrophic conditions. |
2021-03-11 |
2023-08-13 |
mouse |
| Xiaoyan Li, Hue Thi Le, Fuyuki Sato, Tong Ho Kang, Makoto Makishima, Liangjun Zhong, Yi Liu, Lijia Guo, Ujjal K Bhawa. Dec1 deficiency protects the heart from fibrosis, inflammation, and myocardial cell apoptosis in a mouse model of cardiac hypertrophy. Biochemical and biophysical research communications. vol 532. issue 4. 2021-03-11. PMID:32896382. |
in conclusion, a dec1 deficiency protects the heart from perivascular fibrosis, regulates m1/m2 macrophage polarization and reduces cell apoptosis, which may provide a novel insight for the treatment of cardiac hypertrophy. |
2021-03-11 |
2023-08-13 |
mouse |
| Ugo E Pazzaglia, Marcella Reguzzoni, Lavinia Casati, Valeria Sibilia, Guido Zarattini, Mario Raspant. New morphological evidence of the 'fate' of growth plate hypertrophic chondrocytes in the general context of endochondral ossification. Journal of anatomy. vol 236. issue 2. 2021-03-09. PMID:31820452. |
the 'fate' of growth plate hypertrophic chondrocytes has been long debated with two opposing theories: cell apoptosis or survival with transformation into osteogenic cells. |
2021-03-09 |
2023-08-13 |
Not clear |
| Tiago Lazzaretti Fernandes, Andreas H Gomoll, Christian Lattermann, Arnaldo Jose Hernandez, Daniela Franco Bueno, Mariane Tami Aman. Macrophage: A Potential Target on Cartilage Regeneration. Frontiers in immunology. vol 11. 2021-03-08. PMID:32117263. |
synovial inflammation and articular inflammatory environment are the key factor for chondrocytes apoptosis and hypertrophy, ectopic bone formation and oa progression. |
2021-03-08 |
2023-08-13 |
Not clear |
| Shuang Liu, Wen-Chang Sun, Yun-Long Zhang, Qiu-Yue Lin, Jia-Wei Liao, Gui-Rong Song, Xiao-Lei Ma, Hui-Hua Li, Bo Zhan. SOCS3 Negatively Regulates Cardiac Hypertrophy via Targeting GRP78-Mediated ER Stress During Pressure Overload. Frontiers in cell and developmental biology. vol 9. 2021-03-05. PMID:33585485. |
using primary cardiomyocytes and cardiac-specific socs3 knockout (socs3cko) or overexpression mice, we demonstrated that modulation of socs3 level influenced cardiomyocyte hypertrophy, apoptosis and cardiac dysfunction induced by hypertrophic stimuli. |
2021-03-05 |
2023-08-13 |
mouse |
| Shuang Liu, Wen-Chang Sun, Yun-Long Zhang, Qiu-Yue Lin, Jia-Wei Liao, Gui-Rong Song, Xiao-Lei Ma, Hui-Hua Li, Bo Zhan. SOCS3 Negatively Regulates Cardiac Hypertrophy via Targeting GRP78-Mediated ER Stress During Pressure Overload. Frontiers in cell and developmental biology. vol 9. 2021-03-05. PMID:33585485. |
we found that glucose regulatory protein 78 (grp78) was a direct target of socs3, and that overexpression of socs3 inhibited cardiomyocyte hypertrophy and apoptosis through promoting proteasomal degradation of grp78, thereby inhibiting activation of endoplasmic reticulum (er) stress and mitophagy in the heart. |
2021-03-05 |
2023-08-13 |
mouse |
| Chengchuang Zhan, Nan Bai, Min Zheng, Yanyan Wang, Yuanqi Wang, Li Zhang, Jianqiang Li, Guangnan Li, Hongyan Zhao, Guangzhong Liu, Qi Lou, Wen Yang, Tiankai Li, Luyifei Li, Weimin L. Tranilast prevents doxorubicin-induced myocardial hypertrophy and angiotensin II synthesis in rats. Life sciences. vol 267. 2021-03-02. PMID:33383049. |
based on the findings of the present study, the suppression of chymase-dependent ang-ii production and the direct effect of tranilast on the inhibition of apoptosis and fibrosis because of its antioxidant stress capacity may contribute to the protective effect of tranilast against dox-induced myocardial hypertrophy. |
2021-03-02 |
2023-08-13 |
rat |
| Jingsi Zhang, Xiaodan Fu, Li Yang, Hongxin Wen, Lijiao Zhang, Fengyi Liu, Yu Lou, Qian Yang, Yanchun Din. Neohesperidin inhibits cardiac remodeling induced by Ang II in vivo and in vitro. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. vol 129. 2021-03-01. PMID:32531678. |
neohesperidin plays an important role in influencing cell apoptosis, cell growth, tumorigenesis and tumor microenvironment, but the mechanism and role of neohesperidin in cardiac hypertrophy and remodeling caused by angiotensin ii has not been fully elucidated. |
2021-03-01 |
2023-08-13 |
mouse |
| Ying Cheng, Aling Shen, Xiangyan Wu, Zhiqing Shen, Xiaoping Chen, Jiapeng Li, Liya Liu, Xiaoying Lin, Meizhu Wu, Youqin Chen, Jianfeng Chu, Jun Pen. Qingda granule attenuates angiotensin II-induced cardiac hypertrophy and apoptosis and modulates the PI3K/AKT pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. vol 133. 2021-02-24. PMID:33378940. |
qingda granule attenuates angiotensin ii-induced cardiac hypertrophy and apoptosis and modulates the pi3k/akt pathway. |
2021-02-24 |
2023-08-13 |
mouse |
| Ying Cheng, Aling Shen, Xiangyan Wu, Zhiqing Shen, Xiaoping Chen, Jiapeng Li, Liya Liu, Xiaoying Lin, Meizhu Wu, Youqin Chen, Jianfeng Chu, Jun Pen. Qingda granule attenuates angiotensin II-induced cardiac hypertrophy and apoptosis and modulates the PI3K/AKT pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. vol 133. 2021-02-24. PMID:33378940. |
this study aimed to investigate the effects of qdg on hypertension-induced cardiac hypertrophy and apoptosis, as well as explore its underlying mechanisms. |
2021-02-24 |
2023-08-13 |
mouse |
| Ying Cheng, Aling Shen, Xiangyan Wu, Zhiqing Shen, Xiaoping Chen, Jiapeng Li, Liya Liu, Xiaoying Lin, Meizhu Wu, Youqin Chen, Jianfeng Chu, Jun Pen. Qingda granule attenuates angiotensin II-induced cardiac hypertrophy and apoptosis and modulates the PI3K/AKT pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. vol 133. 2021-02-24. PMID:33378940. |
moreover, qdg treatment significantly alleviated the ang ii-induced elevation of the ratio of heart weight to tibia length, as well as cardiac injury, hypertrophy, and apoptosis. |
2021-02-24 |
2023-08-13 |
mouse |