Filtered By:
Condition: Heart Disease
This page shows you your search results in order of date. This is page number 5.
Order by Relevance | Date
Total 126 results found since Jan 2013.
Interference with the expression of S1PR1 or STAT3 attenuates valvular damage due to rheumatic heart disease
Int J Mol Med. 2021 Sep;48(3):179. doi: 10.3892/ijmm.2021.5012. Epub 2021 Jul 23.ABSTRACTRheumatic heart disease (RHD) affects numerous individuals annually; however, its pathogenesis remains unclear. The sphingosine 1‑phosphate receptor 1 (S1PR1) and signal transducer and activator of transcription 3 (STAT3) have recently been shown to be involved in valvular damage via the promotion of the differentiation of T helper 17 (Th17) cells during the development of RHD‑induced valvular damage. The present study investigated whether altering the expression of S1PR1 or STAT3 attenuates valvular damage due to RHD. Inactivated ...
Source: International Journal of Molecular Medicine - July 23, 2021 Category: Molecular Biology Authors: Shenglin Xian Ang Chen Yunjiao Wu Hong Wen Chuanghong Lu Feng Huang Zhiyu Zeng Source Type: research
HDAC1 and 2 regulate endothelial VCAM-1 expression and atherogenesis by suppressing methylation of the GATA6 promoter
Conclusions: HDAC1/2 contributes to VCAM-1 expression and atherosclerosis by suppressing STAT3 acetylation-dependent GATA6 promoter methylation. These findings may provide a rationale for HDAC1/2-targeting therapy in atherosclerotic heart disease.
Source: Theranostics - April 19, 2021 Category: Molecular Biology Authors: Chengxiu Hu, Kai Peng, Qianqian Wu, Yiying Wang, Xing Fan, Dai-Min Zhang, Anthony G. Passerini, ChongXiu Sun Tags: Research Paper Source Type: research
Crosstalk between the activated Slit2 –Robo1 pathway and TGF‐β1 signalling promotes cardiac fibrosis
ConclusionsThe Slit2 –Robo1 signalling pathway interfered with the TGF‐β1/Smad pathway and promoted cardiac fibrosis. Blockade of Slit2–Robo1 might be a new treatment for cardiac fibrosis.
Source: ESC Heart Failure - January 25, 2021 Category: Cardiology Authors: Yunqi Liu,
Ziwei Yin,
Xueqin Xu,
Chen Liu,
Xiaoying Duan,
Qinlan Song,
Ying Tuo,
Cuiping Wang,
Jing Yang,
Shengli Yin Tags: Original Research Article Source Type: research
Schisandrin B Protects against Acute Ethanol-Induced Cardiac Injury by Downregulating Autophagy via the NOX4/ROS Pathway
Conclusion: These results highlight that NOX4 is a critical mediator of ROS and elaborate the role of the NOX4/ROS axis in the effect of schisandrin B on autophagy and autophagy-mediated apoptosis in acute ethanol exposure, which suggests a therapeutic strategy for acute alcoholic cardiomyopathy.Pharmacology
Source: Pharmacology - January 22, 2021 Category: Drugs & Pharmacology Source Type: research
Crosstalk between the activated Slit2 –Robo1 pathway and TGF‐β1 signalling promotes cardiac fibrosis
ConclusionsThe Slit2 –Robo1 signalling pathway interfered with the TGF‐β1/Smad pathway and promoted cardiac fibrosis. Blockade of Slit2–Robo1 might be a new treatment for cardiac fibrosis.
Source: ESC Heart Failure - November 24, 2020 Category: Cardiology Authors: Yunqi Liu,
Ziwei Yin,
Xueqin Xu,
Chen Liu,
Xiaoying Duan,
Qinlan Song,
Ying Tuo,
Cuiping Wang,
Jing Yang,
Shengli Yin Tags: Original Research Article Source Type: research
Nicotine-induced adrenal beta-arrestin1 upregulation mediates tobacco-related hyperaldosteronism leading to cardiac dysfunction.
CONCLUSION: Adrenal βarrestin1 upregulation is one of the mechanisms by which tobacco compounds, like nicotine, promote cardio-toxic hyperaldosteronism in vitro and in vivo. Thus, adrenal βarrestin1 represents a novel therapeutic target for tobacco-related heart disease prevention or mitigation.
PMID: 32547713 [PubMed]
Source: World Journal of Cardiology - May 25, 2020 Category: Cardiology Authors: Cora N, Ghandour J, Pollard CM, Desimine VL, Ferraino KE, Pereyra JM, Valiente R, Lymperopoulos A Tags: World J Cardiol Source Type: research
Elevated Aldolase 1A, retrogene 1 expression induces cardiac apoptosis in rat experimental autoimmune myocarditis model.
Abstract
Acute myocarditis is an unpredictable heart disease, which is caused by inflammation-associated cell death. Although viral infection and drug exposure are known to induce acute myocarditis, the molecular basis for its development remains undefined. Using proteomics and molecular analyses in myosin-induced rat experimental autoimmune myocarditis (EAM), we identified that elevated expression of aldolase 1A, retrogene 1 (Aldoart1) is critical to induce mitochondrial dysfunction and acute myocarditis development. Here, we demonstrate that cardiac cell death is associated with increased expressions of pro-apop...
Source: Canadian Journal of Physiology and Pharmacology - January 29, 2020 Category: Drugs & Pharmacology Authors: Choi S, Chung JH, Nam MH, Bang E, Hong KS, Kim YH, Seo JB, Chi SG Tags: Can J Physiol Pharmacol Source Type: research
Pituitary adenylate cyclase-activating polypeptide ameliorates radiation-induced cardiac injury.
Authors: Li H, Cao L, Yi PQ, Xu C, Su J, Chen PZ, Li M, Chen JY
Abstract
Radiation-induced heart disease (RIHD) is a common sequelae of thoracic irradiation. Currently, there is no effective prevention and treatment strategy. Oxidative stress is associated with the development of RIHD. Pituitary adenylate cyclase-activating polypeptide 38 (PACAP38) has been defined as the multipotent properties of cytoprotective effect on its anti-apoptotic and antioxidant activities. Here, we set to investigate whether PACAP38 plays a role in attenuating RIHD. We established radiation-related cardiac injury models using 6MV X-ray ...
Source: American Journal of Translational Research - November 20, 2019 Category: Research Tags: Am J Transl Res Source Type: research
TBX3 deficiency accelerates apoptosis in cardiomyoblasts through regulation of P21 expression
In conclusion, we demonstrated that TBX3 deficiency accelerated apoptosis via directly regulating P21 expression in senescent cardiomyoblasts.
Source: Life Sciences - November 6, 2019 Category: Biology Source Type: research
miR-370 inhibits the oxidative stress and apoptosis of cardiac myocytes induced by hydrogen peroxide by targeting FOXO1.
Authors: Qiu Z, Wang L, Mao H, Xu F, Sun B, Lian X, Wang J, Kong F, Wang L, Chen Y
Abstract
Myocardial infarction, one of the main factors that threatens human health, leads to cardiac cell death. Myocardial cells suffer ischemia and hypoxia for a long period of time, which can lead to irreversible cell death or apoptosis and cardiac dysfunction. MicroRNAs (miRs) have been reported to play an important role in a wide range of biological processes in cardiac myocytes, which respond to inflammation and oxidative stress. The aim of the present study was to investigate the effect of miR-370 on oxidative stress and apop...
Source: Experimental and Therapeutic Medicine - September 28, 2019 Category: General Medicine Tags: Exp Ther Med Source Type: research
Adenine decreases hypertrophic effects through interleukin-18 receptor.
In this study, IL-18 induced cardiomyoblast hypertrophy through IL-18R upregulation, which was found to be related to p38 MAPK and PI3 kinase signaling. Adenine, but not AuNPs, showed antihypertrophic effects possibly because of decreased levels of signaling.
PMID: 31535629 [PubMed - in process]
Source: The Chinese Journal of Physiology - September 20, 2019 Category: Physiology Tags: Chin J Physiol Source Type: research
The effects of Tel2 on cardiomyocyte survival
Publication date: 1 September 2019Source: Life Sciences, Volume 232Author(s): Naaiko Yorichika, Yuichi Baba, Briana K. Shimada, Manoj Thakore, Sharon M. Wong, Motoi Kobayashi, Jason K. Higa, Takashi MatsuiAbstractAimsOverexpression of the mechanistic target of rapamycin (mTOR), a member of the PIKK (phosphoinositide kinase-related kinase) family, protects cardiomyocytes from cell death induced by pathological stimuli such as ischemia. We previously reported that posttranslational modification of mTOR plays an important role in regulating cardiac mTOR expression. The aim of this study was to see if Tel2 (telomere maintenanc...
Source: Life Sciences - July 25, 2019 Category: Biology Source Type: research
miR-17 regulates the proliferation and apoptosis of endothelial cells in coronary heart disease via targeting insulin-like-growth factor 1
Publication date: Available online 20 June 2019Source: Pathology - Research and PracticeAuthor(s): Zhongpu Chen, Xiaodong Pan, Zulong Sheng, Gaoliang Yan, Long Chen, Genshan MaAbstractCoronary heart disease (CHD) is one of the main risks of death, which is mainly caused by coronary arteries arteriosclerosis. The present study aims to investigate the potential roles of miR-17 in CHD. In the present study, Human umbilical vascular endothelial cells (HUVECs) were treated with oxidized low density lipoprotein (ox-LDL). qRT-PCR and western blot were used to examine the mRNA and protein levels, respectively. CCK-8 and flow cytom...
Source: Pathology Research and Practice - June 22, 2019 Category: Pathology Source Type: research
Tangshen Formula Alleviates Hepatic Steatosis by Inducing Autophagy Through the AMPK/SIRT1 Pathway
Conclusion
In conclusion, the present study demonstrated that autophagy was involved in relieving the effects of TSF against NAFLD, which were mediated by the AMPK/SIRT1 pathway (Figure 7D). These findings may improve our current understanding of the role of TSF in treating hepatic steatosis and provide an experimental basis for the clinical application of TSF in NAFLD and its related metabolic syndrome.
Ethics Statement
This study was carried out in accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. The protocol was approved by the Ethics Co...
Source: Frontiers in Physiology - April 25, 2019 Category: Physiology Source Type: research
