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Condition: Heart Failure
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Total 253 results found since Jan 2013.
Silencing Survivin: a Key Therapeutic Strategy for Cardiac Hypertrophy
In this study, we investigated the involvement of SURV in intracellular signaling of hypertrophic cardiomyocytes and the impact of its transcriptional silencing, laying the foundation for novel target gene therapy in cardiac hypertrophy. Oligonucleotide-based molecules, like theranostic optical nanosensors (molecular beacons) and siRNAs, targeting SURV and OPN mRNAs, were developed. Their diagnostic and therapeutic potential was evaluated in vitro in hypertrophic FGF23-induced human cardiomyocytes and in vivo in transverse aortic constriction hypertrophic mouse model. Engineered erythrocyte was used as shuttle to selective...
Source: Journal of Cardiovascular Translational Research - August 18, 2021 Category: Cardiology Source Type: research
Zinc finger and BTB domain-containing protein 20 aggravates angiotensin II-induced cardiac remodeling via the EGFR-AKT pathway
J Mol Med (Berl). 2021 Jul 7. doi: 10.1007/s00109-021-02103-0. Online ahead of print.ABSTRACTZinc finger and BTB domain-containing protein 20 (ZBTB20) play an important role in glucose and lipid homeostasis. ZBTB20 was shown to be a crucial protein for the maintenance of cardiac contractile function. However, the role of ZBTB20 in cardiac response remodeling has not been elucidated. Thus, this study aimed to explore the role of ZBTB20 in cardiac remodeling following angiotensin II insult. Mice were subjected to angiotensin II infusion to induce a cardiac adverse remodeling model. An adeno-associated virus (AAV) 9 system wa...
Source: Molecular Medicine - July 7, 2021 Category: Molecular Biology Authors: Fangfang Li Miaomiao Du Yiming Yang Zhu Wang Hu Zhang Xiaoyu Wang Qing Li Source Type: research
Radiation-induced lipoprotein-associated phospholipase A2 increases lysophosphatidylcholine and induces endothelial cell damage
In this study, radiation-induced LPC accumulation in human aortic endothelial cells (HAECs) increased reactive oxygen species (ROS) production and senescence-associated-beta-galactosidase staining, in addition to decreasing their tube-forming ability. Knockdown of lipoprotein-associated phospholipase A2 (Lp-PLA2) with small interfering RNA (siRNA) inhibited the increased LPC production induced by radiation, and reduced the radiation-induced cell damage produced by ROS and oxidized low-density lipoprotein (LDL). Lp-PLA2 depletion abolished the induction of proinflammatory factors, such as interleukin 1β, tumor necrosis fac...
Source: Toxicology - July 3, 2021 Category: Toxicology Authors: So-Ra Kim Jong-Ik Heo Jeong-Woo Park Chang-Mo Kang Kwang Seok Kim Source Type: research
Dapagliflozin alleviates cardiac fibrosis through suppressing EndMT and fibroblast activation via AMPK α/TGF-β/Smad signalling in type 2 diabetic rats
This study aimed to evaluate the effect of SGLT2 inhibitor dapagliflozin (DAPA) on DCM especially for cardiac fibrosis and explore the underlying mechanism. In vivo, the model of type 2 diabetic rats was built with high-fat feeding and streptozotocin injection. Untreated diabetic rats showed cardiac dysfunction, increased myocardial fibrosis and EndMT, which was attenuated after treatment with DAPA and metformin. In vitro, HUVECs and primary cardiac fibroblasts were treated with DAPA and exposed to high glucose (HG). HG-induced EndMT in HUVECs and collagen secretion of fibroblasts were markedly inhibited by DAPA. Up-regula...
Source: J Cell Mol Med - June 25, 2021 Category: Molecular Biology Authors: Jingjing Tian Mingjun Zhang Mengying Suo Dian Liu Xuyang Wang Ming Liu Jinyu Pan Tao Jin Fengshuang An Source Type: research
P53 mediates the stimulation of mitochondrial reactive oxygen species and suppression of 18F-FDG uptake and glycolysis in isoprenaline-treated H9C2 cardiomyocytes
Conclusions: These findings demonstrate that ISO treatment decreases cardiomyocyte 18F-FDG uptake by downregulating glycolytic flux and further reveals that ROS-p53 signaling plays a critical role in this metabolic response.
Source: Journal of Nuclear Medicine - May 18, 2021 Category: Nuclear Medicine Authors: Lee, J. H., Kim, D. H., Kim, M., Cho, Y. S., Jung, K.-H., LEE, K.-H. Tags: Cardiovascular Basic Science Source Type: research
FABP5 Deficiency Impairs Mitochondrial Function and Aggravates Pathological Cardiac Remodeling and Dysfunction
Cardiovasc Toxicol. 2021 Apr 30. doi: 10.1007/s12012-021-09653-2. Online ahead of print.ABSTRACTFatty acid-binding protein 5 (FABP5) is an important member of the FABP family and plays a vital role in the metabolism of fatty acids. However, few studies have examined the role of FABP5 in pathological cardiac remodeling and heart failure. The aim of this study was to explore the role of FABP5 in transverse aortic constriction (TAC)-induced pathological cardiac remodeling and dysfunction in mice. Quantitative RT-PCR (qRT-PCR) and western blotting (WB) analysis showed that the levels of FABP5 mRNA and protein, respectively, we...
Source: Cardiovascular Toxicology - April 30, 2021 Category: Cardiology Authors: Shanquan Gao Guoqi Li Yihui Shao Zhipeng Wei Shan Huang Feiran Qi Yao Jiao Yulin Li Congcong Zhang Jie Du Source Type: research
