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Condition: Heart Failure
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Total 253 results found since Jan 2013.
miR-181b targets semaphorin 3A to mediate TGF-β–induced endothelial-mesenchymal transition related to atrial fibrillation
Atrial fibrosis is an essential contributor to atrial fibrillation (AF). It remains unclear whether atrial endocardial endothelial cells (AEECs) that undergo endothelial-mesenchymal transition (EndMT) are among the sources of atrial fibroblasts. We studied human atria, TGF-β–treated human AEECs, cardiac-specific TGF-β–transgenic mice, and heart failure rabbits to identify the underlying mechanism of EndMT in atrial fibrosis. Using isolated AEECs, we found that miR-181b was induced in TGF-β–treated AEECs, which decreased semaphorin 3A (Sema3A) and increased EndMT markers, and these effects could be reversed by a mi...
Source: Journal of Clinical Investigation - July 1, 2022 Category: Biomedical Science Authors: Ying-Ju Lai, Feng-Chun Tsai, Gwo-Jyh Chang, Shang-Hung Chang, Chung-Chi Huang, Wei-Jan Chen, Yung-Hsin Yeh Source Type: research
Oxidative stress regulates cardiomyocyte energy metabolism through the IGF2BP2-dynamin2 signaling pathway
CONCLUSION: Oxidative stress can induce cardiomyocyte apoptosis through the IGF2BP2-dynamin2 pathway. Inhibition of IGF2BP2 expression significantly improves the fibrosis and remodeling that occurs in ischemic myocardium.PMID:35940126 | DOI:10.1016/j.bbrc.2022.07.089
Source: Biochemical and Biophysical Research communications - August 8, 2022 Category: Biochemistry Authors: Juncheng Wang Shan Li Huajiong Yu Danchen Gao Source Type: research
Infusion of two-dose mesenchymal stem cells is more effective than a single dose in a dilated cardiomyopathy rat model by upregulating indoleamine 2,3-dioxygenase expression
CONCLUSIONS: Administration of two-dose hUCMSCs has better therapeutic effects than single-dose therapy for inhibiting myocardial inflammation to improve LV function in DCM rats. These effects are associated with upregulating IDO expression and its systemic anti-inflammatory activities.PMID:35962420 | DOI:10.1186/s13287-022-03101-w
Source: Cell Research - August 12, 2022 Category: Cytology Authors: Chenyi Gong Lei Chang Xuan Sun Yu Qi Rong Huang Ke Chen Bin Wang Lina Kang Lian Wang Biao Xu Source Type: research
Selenium alleviates heart remodeling through Sirt1/AKT/GSK-3 β pathway
In this study, we explored the effects of selenium on heart failure and its possible mechanism. The heart failure models were induced by aortic banding and isoproterenol. H&E, TUNEL and PSR staining were performed to detect the degree of cardiomyocyte hypertrophy, apoptosis rates and heart fibrosis, respectively. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect different mRNA levels, and western blot was applied to assess the expressions of relative proteins. Immunofluorescence staining was used to evaluate α-SMA density. We first found that treatment of selenium alleviated heart fibrosis ...
Source: International Immunopharmacology - August 20, 2022 Category: Allergy & Immunology Authors: Cui Shengyu Luo Yinhua Li Yuanhong Zhao Jinbo Fang Can Xia Hao Zhang Changjiang Source Type: research
Protections of transcription factor BACH2 and natural product myricetin against pathological cardiac hypertrophy and dysfunction
This study aims to explore the role of BACH2, a member of the basic region leucine zipper transcription factor family, in cardiac hypertrophy and failure. Transverse aortic constriction surgery was operated to induce cardiac hypertrophy and failure in mice. BACH2 was overexpressed in mice through tail vein injection of AAV9-Bach2. Mice with systemic or cardiac-specific knockdown of Bach2 were adopted. Neonatal rat ventricular myocytes (NRVMs) were isolated and infected with lentivirus to overexpress Bach2 or transfected with siRNA to knock down Bach2. Our data showed that overexpression of BACH2 ameliorated TAC-induced car...
Source: Frontiers in Physiology - August 29, 2022 Category: Physiology Source Type: research
Pyrroloquinoline quinone modulates YAP-related anti-ferroptotic activity to protect against myocardial hypertrophy
Conclusion: PQQ can regulate the pathogenesis of myocardial hypertrophy through the induction of YAP-related anti-ferroptotic activity, highlighting the potential value of PQQ as a novel therapeutic agent capable of slowing or preventing the progression of myocardial hypertrophy and thus delaying the onset of heart failure.
Source: Frontiers in Pharmacology - September 27, 2022 Category: Drugs & Pharmacology Source Type: research
Melatonin alleviates arginine vasopressin-induced cardiomyocyte apoptosis via increasing Mst1-Nrf2 pathway activity to reduce oxidative stress
In this study, high AVP doses were found to induce H9c2 cardiomyoblast apoptosis, demonstrated by increased terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells, pro-apoptotic B-cell lymphoma-2 (Bcl-2)-associated X protein (Bax) up-regulation, and anti-apoptotic Bcl-2 downregulation. This AVP-induced apoptotic increase, along with lowered cell viability, was also associated with higher reactive oxygen species (ROS) levels and lowered mitochondrial membrane potentials (MMP), which were all reversed upon Mel administration. Further investigations found that apoptosis, ROS, and MMP outcomes unde...
Source: Biochemical Pharmacology - October 2, 2022 Category: Drugs & Pharmacology Authors: Shuang Chen You Li Shuai Fu Yang Li Chao Wang Ping Sun Hairu Li Jiawei Tian Guo-Qing Du Source Type: research
BRD4 Silencing Protects Angiotensin II-Induced Cardiac Hypertrophy by Inhibiting TLR4/NF- < em > κ < /em > B and Activating Nrf2-HO-1 Pathways
CONCLUSION: Our results speculate that the BRD4/TLR4 axis might be a promising strategy for treating cardiovascular diseases with cardiac hypertrophy, including HF.PMID:36247184 | PMC:PMC9553838 | DOI:10.1155/2022/8372707
Source: Cardiology Research and Practice - October 17, 2022 Category: Cardiology Authors: Ming Fang Jun Luo Xi Zhu Yingbiao Wu Xinming Li Source Type: research
< em > SOX17 < /em > Enhancer Variants Disrupt Transcription Factor Binding And Enhancer Inactivity Drives Pulmonary Hypertension
CONCLUSIONS: Common PAH risk variants upstream of the SOX17 promoter reduce endothelial SOX17 expression, at least in part, through differential binding of HOXA5 and ROR-α. Reduced SOX17 expression results in disturbed hPAEC function and PAH. Existing drug compounds can reverse the disturbed SOX17 pulmonary endothelial transcriptomic signature.PMID:37066790 | DOI:10.1161/CIRCULATIONAHA.122.061940
Source: Circulation - April 17, 2023 Category: Cardiology Authors: Rachel Walters Eleni Vasilaki Jurjan Aman Chien-Nien Chen Yukyee Wu Olin D Liang Ali Ashek Olivier Dubois Lin Zhao Farah Sabrin In ês Cebola Jorge Ferrer Nicholas W Morrell James R Klinger Martin R Wilkins Lan Zhao Christopher J Rhodes Source Type: research
