| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Qi Zhang, Danyang Li, Xue Dong, Xiaowen Zhang, Junwu Liu, Lili Peng, Bo Meng, Qi Hua, Xinyu Pei, Lu Zhao, Xiaoxi Hu, Yang Zhang, Zhenwei Pan, Yanjie Lu, Baofeng Yan. LncDACH1 promotes mitochondrial oxidative stress of cardiomyocytes by interacting with sirtuin3 and aggravates diabetic cardiomyopathy. Science China. Life sciences. 2021-10-20. PMID:34668131. |
knockout of lncdach1 reduced mitochondrial oxidative stress, cell apoptosis, cardiac fibrosis and hypertrophy, and improved cardiac function in dcm mice. |
2021-10-20 |
2023-08-13 |
mouse |
| Xiaomin Hu, Peng Wu, Bojiang Liu, Yuheng Lang, Tong L. RNA-binding protein CELF1 promotes cardiac hypertrophy via interaction with PEBP1 in cardiomyocytes. Cell and tissue research. 2021-10-20. PMID:34669021. |
based on transverse aortic constriction-induced cardiac hypertrophy model, celf1 deficiency markedly ameliorated cardiac hypertrophy, cardiac fibrosis, oxidative stress, and apoptosis. |
2021-10-20 |
2023-08-13 |
Not clear |
| Xiaomin Hu, Peng Wu, Bojiang Liu, Yuheng Lang, Tong L. RNA-binding protein CELF1 promotes cardiac hypertrophy via interaction with PEBP1 in cardiomyocytes. Cell and tissue research. 2021-10-20. PMID:34669021. |
inhibition of celf1 attenuates pathological cardiac hypertrophy, oxidative stress, and apoptosis, thus could be a potential therapeutic strategy of pathological cardiac hypertrophy. |
2021-10-20 |
2023-08-13 |
Not clear |
| Wang-Soo Lee, Jaetaek Ki. Application of Animal Models in Diabetic Cardiomyopathy. Diabetes & metabolism journal. vol 45. issue 2. 2021-10-15. PMID:33813812. |
the underlying pathomechanism of diacm is partially understood, but accumulating evidence suggests that metabolic derangements, oxidative stress, increased myocardial fibrosis and hypertrophy, inflammation, enhanced apoptosis, impaired intracellular calcium handling, activation of the renin-angiotensin-aldosterone system, mitochondrial dysfunction, and dysregulation of micrornas, among other factors, are involved. |
2021-10-15 |
2023-08-13 |
Not clear |
| Heqin Zhan, Feng Huang, Qian Niu, Mingli Jiao, Xumeng Han, Kaina Zhang, WenZhuo Ma, Shan Mi, Shiyu Guo, Zhenghang Zha. Downregulation of miR-128 Ameliorates Ang II-Induced Cardiac Remodeling via SIRT1/PIK3R1 Multiple Targets. Oxidative medicine and cellular longevity. vol 2021. 2021-10-15. PMID:34646427. |
in vitro experiments of cardiac hypertrophy, apoptosis, and aberrant autophagy were performed in cultured cells after ang ii treatment or transfection of mir-128 antagomir. |
2021-10-15 |
2023-08-13 |
mouse |
| Heqin Zhan, Feng Huang, Qian Niu, Mingli Jiao, Xumeng Han, Kaina Zhang, WenZhuo Ma, Shan Mi, Shiyu Guo, Zhenghang Zha. Downregulation of miR-128 Ameliorates Ang II-Induced Cardiac Remodeling via SIRT1/PIK3R1 Multiple Targets. Oxidative medicine and cellular longevity. vol 2021. 2021-10-15. PMID:34646427. |
our results showed that chronic ang ii delivery for 28 days induced cardiac dysfunction, hypertrophy, fibrosis, apoptosis, and oxidative stress in the mice, while the mir-128 expression was notably enhanced in the left ventricle. |
2021-10-15 |
2023-08-13 |
mouse |
| Heqin Zhan, Feng Huang, Qian Niu, Mingli Jiao, Xumeng Han, Kaina Zhang, WenZhuo Ma, Shan Mi, Shiyu Guo, Zhenghang Zha. Downregulation of miR-128 Ameliorates Ang II-Induced Cardiac Remodeling via SIRT1/PIK3R1 Multiple Targets. Oxidative medicine and cellular longevity. vol 2021. 2021-10-15. PMID:34646427. |
silencing mir-128 in the hearts of mice ameliorated ang ii-induced cardiac dysfunction, hypertrophy, fibrosis apoptosis, and oxidative stress injury. |
2021-10-15 |
2023-08-13 |
mouse |
| Heqin Zhan, Feng Huang, Qian Niu, Mingli Jiao, Xumeng Han, Kaina Zhang, WenZhuo Ma, Shan Mi, Shiyu Guo, Zhenghang Zha. Downregulation of miR-128 Ameliorates Ang II-Induced Cardiac Remodeling via SIRT1/PIK3R1 Multiple Targets. Oxidative medicine and cellular longevity. vol 2021. 2021-10-15. PMID:34646427. |
in conclusion, downregulation of mir-128 ameliorates ang ii-provoked cardiac oxidative stress, hypertrophy, fibrosis, apoptosis, and dysfunction in mice, likely through targeting on pik3r1/akt/mtorc1 and/or sirt1/p53 pathways. |
2021-10-15 |
2023-08-13 |
mouse |
| Chi-Yung Chai, I-Chun Tai, Rui Zhou, Junlong Song, Chaoying Zhang, Shengrong Su. MicroRNA-9-5p inhibits proliferation and induces apoptosis of human hypertrophic scar fibroblasts through targeting peroxisome proliferator-activated receptor β. Biology open. vol 9. issue 12. 2021-10-12. PMID:33355167. |
microrna-9-5p inhibits proliferation and induces apoptosis of human hypertrophic scar fibroblasts through targeting peroxisome proliferator-activated receptor β. |
2021-10-12 |
2023-08-13 |
human |
| Anita Dittrich, Henrik Lauridse. Cryo-injury Induced Heart Regeneration in the Axolotl and Echocardiography and Unbiased Quantitative Histology to Evaluate Regenerative Progression. Journal of visualized experiments : JoVE. issue 171. 2021-10-08. PMID:34028427. |
however, the model does not relate well to clinical situations in which tissue damage, apoptosis, necrosis, fibrosis, and hypertrophy are all key detrimental consequences of ischemia-induced myocardial infarctions rather than tissue removal. |
2021-10-08 |
2023-08-13 |
Not clear |
| Xiang Wang, Xin-Xin Chen, Hai-Tao Yu, Yi Tan, Qian Lin, Bradley B Keller, Yang Zheng, Lu Ca. Engineered cardiac tissues: a novel in vitro model to investigate the pathophysiology of mouse diabetic cardiomyopathy. Acta pharmacologica Sinica. vol 42. issue 6. 2021-10-07. PMID:33037406. |
we treated ects composed of neonatal murine cardiac cells with ages and observed age-related functional, cellular, and molecular alterations: (1) ages (150 µg/ml) did not cause acute cytotoxicity, which displayed as necrosis detected by medium ldh release or apoptosis detected by cleaved caspase 3 and tunel staining, but negatively impacted ect function on treatment day 9; (2) ages treatment significantly increased the markers of fibrosis (tgf-β, α-sma, ctgf, collagen i-α1, collagen iii-α1, and fn1) and hypertrophy (nppa and myh7); (3) ages treatment significantly increased ect oxidative stress markers (3-nt, 4-hne, ho-1, cat, and sod2) and inflammation response markers (pai-1, tnf-α, nf-κb, and icam-1); and (4) age-induced pathogenic responses were all attenuated by pre-application of age receptor antagonist fps-zm1 (20 µm) or the antioxidant glutathione precursor n-acetylcysteine (5 mm). |
2021-10-07 |
2023-08-13 |
mouse |
| Daniel Jakubik, Alex Fitas, Ceren Eyileten, Joanna Jarosz-Popek, Anna Nowak, Pamela Czajka, Zofia Wicik, Harald Sourij, Jolanta M Siller-Matula, Salvatore De Rosa, Marek Postul. MicroRNAs and long non-coding RNAs in the pathophysiological processes of diabetic cardiomyopathy: emerging biomarkers and potential therapeutics. Cardiovascular diabetology. vol 20. issue 1. 2021-10-06. PMID:33639953. |
this article will review the different mirnas and lncrna studied in the context of dm, including type 1 and type 2 diabetes and the contribution of pathophysiological mechanisms including inflammatory response, oxidative stress, apoptosis, hypertrophy and fibrosis to the development of dcm . |
2021-10-06 |
2023-08-13 |
Not clear |
| Wenjing Fan, Beibei Zhang, Caiqin Wu, Hui Wu, Jing Wu, Shijia Wu, Jinxian Zhang, Xinhua Yang, Li Yang, Zhibi Hu, Xiaojun W. Plantago asiatica L. seeds extract protects against cardiomyocyte injury in isoproterenol- induced cardiac hypertrophy by inhibiting excessive autophagy and apoptosis in mice. Phytomedicine : international journal of phytotherapy and phytopharmacology. vol 91. 2021-10-06. PMID:34371252. |
plantago asiatica l. seeds extract protects against cardiomyocyte injury in isoproterenol- induced cardiac hypertrophy by inhibiting excessive autophagy and apoptosis in mice. |
2021-10-06 |
2023-08-13 |
mouse |
| Wenjing Fan, Beibei Zhang, Caiqin Wu, Hui Wu, Jing Wu, Shijia Wu, Jinxian Zhang, Xinhua Yang, Li Yang, Zhibi Hu, Xiaojun W. Plantago asiatica L. seeds extract protects against cardiomyocyte injury in isoproterenol- induced cardiac hypertrophy by inhibiting excessive autophagy and apoptosis in mice. Phytomedicine : international journal of phytotherapy and phytopharmacology. vol 91. 2021-10-06. PMID:34371252. |
cardiomyocyte autophagy and apoptosis play an important role in the process of cardiac hypertrophic response. |
2021-10-06 |
2023-08-13 |
mouse |
| Tung-Sheng Chen, Shou-Ying Chuang, Chia-Yao Shen, Tsung-Jung Ho, Ruey-Lin Chang, Yu-Lan Yeh, Chia-Hua Kuo, B Mahalakshmi, Wei-Wen Kuo, Chih-Yang Huan. Antioxidant Sirt1/Akt axis expression in resveratrol pretreated adipose-derived stem cells increases regenerative capability in a rat model with cardiomyopathy induced by diabetes mellitus. Journal of cellular physiology. vol 236. issue 6. 2021-10-04. PMID:33421145. |
compared to the sham, dm induces pathological pathways (including fibrosis, hypertrophy, and apoptosis) and suppresses survival as well as the ampk/sirt1 axis in the dm group. |
2021-10-04 |
2023-08-13 |
rat |
| Ping Fan, Likun Zhang, Tianyu Cheng, Jing Wang, Junyun Zhou, Li Zhao, Cuie Hua, Quan Xi. MiR-590-5p inhibits pathological hypertrophy mediated heart failure by targeting RTN4. Journal of molecular histology. vol 52. issue 5. 2021-10-04. PMID:34406553. |
injection of aav-mir-590-5p attenuated myocardium hypertrophy and myocyte apoptosis. |
2021-10-04 |
2023-08-13 |
mouse |
| Ping Fan, Likun Zhang, Tianyu Cheng, Jing Wang, Junyun Zhou, Li Zhao, Cuie Hua, Quan Xi. MiR-590-5p inhibits pathological hypertrophy mediated heart failure by targeting RTN4. Journal of molecular histology. vol 52. issue 5. 2021-10-04. PMID:34406553. |
in conclusion, mir-590-5p modulates myocardium hypertrophy and myocyte apoptosis in hf by downregulating rtn4. |
2021-10-04 |
2023-08-13 |
mouse |
| Ludger Hauck, Keith Dadson, Shelly Chauhan, Daniela Grothe, Filio Billi. Inhibiting the Pkm2/b-catenin axis drives in vivo replication of adult cardiomyocytes following experimental MI. Cell death and differentiation. vol 28. issue 4. 2021-10-01. PMID:33288902. |
we found a lack of cardiac hypertrophy or expression of the fetal gene program in pkm2koi mice post mi, as compared to vehicle control animals (p < 0.01), correlating with smaller infarct size, improved mitochondrial (mt) function, enhanced angiogenesis, reduced degree of cm apoptosis, and reduced oxidative stress post mi. |
2021-10-01 |
2023-08-13 |
mouse |
| Yimin Liang, Renpeng Zhou, Xiujun Fu, Chen Wang, Danru Wan. HOXA5 counteracts the function of pathological scar-derived fibroblasts by partially activating p53 signaling. Cell death & disease. vol 12. issue 1. 2021-10-01. PMID:33414417. |
in this study, we first demonstrated that hoxa5 overexpression in hypertrophic scar-or keloids-derived fibroblasts decreased cell proliferation, migration and collagen synthesis, whereas increased cell apoptosis. |
2021-10-01 |
2023-08-13 |
Not clear |
| Jingang Sun, Cuicui Zhang, Zhigang Zhan. Atorvastatin attenuates cardiac hypertrophy through AMPK/miR-143-3p/Bcl2 axis. Archives of physiology and biochemistry. vol 127. issue 5. 2021-09-30. PMID:31353965. |
taken together, the data indicated that mir-143-3p aggravated cardiac hypertrophy by inducing cardiomyocytes apoptosis through inhibiting bcl2 expression. |
2021-09-30 |
2023-08-13 |
rat |