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Condition: Heart Failure
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Total 161 results found since Jan 2013.
LRRC8A contributes to angiotensin II-induced cardiac hypertrophy by interacting with NADPH oxidases via the C-terminal leucine-rich repeat domain.
Abstract
Cardiac hypertrophy, an important cause of heart failure, is characterized by an increase in heart weight, the ventricular wall, and cardiomyocyte volume. The volume regulatory anion channel (VRAC) is an important regulator of cell volume. However, its role in cardiac hypertrophy remains unclear. The purpose of this study was to investigate the effect of leucine-rich repeat-containing 8A (LRRC8A), an essential component of the VRAC, on angiotensin II (AngII)-induced cardiac hypertrophy. Our results showed that LRRC8A expression, NADPH oxidase activity, and reactive oxygen species (ROS) production were inc...
Source: Free Radical Biology and Medicine - January 27, 2021 Category: Biology Authors: Huo C, Liu Y, Li X, Xu R, Jia X, Hou L, Wang X Tags: Free Radic Biol Med Source Type: research
Endothelial Klf2-Foxp1-TGF β signal mediates the inhibitory effects of simvastatin on maladaptive cardiac remodeling
Conclusions: We conclude that cardiac microvasculature ECs are important in the modulation of pressure overload induced maladaptive cardiac remodeling and dysfunction, and the endothelial Klf2-TGFβ1 or Klf2-Foxp1-TGFβ1 pathway mediates the preventive effects of simvastatin. This study demonstrates a novel mechanism of the non-cholesterol lowering effects of simvastatin for HF prevention.
Source: Theranostics - January 15, 2021 Category: Molecular Biology Authors: Hongda Li, Yanfang Wang, Jiwen Liu, Xiaoli Chen, Yunhao Duan, Xiaoyu Wang, Yajing Shen, Yashu Kuang, Tao Zhuang, Brain Tomlinson, Paul Chan, Zuoren Yu, Yu Cheng, Lin Zhang, Zhongmin Liu, Yuzhen Zhang, Zhenlin Zhao, Qi Zhang, Jie Liu Tags: Research Paper Source Type: research
The mechanism of BAF60c in myocardial metabolism through the PGC1 α/PPARα/mTOR signaling pathway in rats with heart failure.
This study explored the mechanism of BAF60c in heart failure (HF). Fetal/adult rat models of HF were established, and the levels of cardiac contractile proteins and energy metabolism-, oxidative metabolism- and glycolysis-related factors were detected. Overexpression/siRNA BAF60c plasmids were injected into adult HF rats to estimate myocardial glucose uptake, high-energy phosphate contents, mitochondrial function, and cell proliferation and apoptosis. The overexpression/siRNA BAF60c plasmids were transfected into cardiac hypertrophic H9C2 cells to explore the in vitro effects. The interaction of BAF60c and PGC1α was detec...
Source: Biochemistry and Cell Biology - November 27, 2020 Category: Biochemistry Authors: Chen Q, Chen L, Jian J, Li J, Zhang X Tags: Biochem Cell Biol Source Type: research
NRF2 in Cardiovascular Diseases: a Ray of Hope!
AbstractHeart failure is a worldwide pandemic influencing 26 million individuals worldwide and is expanding. Imbalanced redox homeostasis in cardiac cells alters the structure and function of the cells, which leads to contractile dysfunction, myocardial hypertrophy, and fibrosis in chronic heart failure. Various targets and agents acting on these such as siRNA, miRNA, interleukin-1, opioids, vasodilators, and SGLT2 inhibitors are being evaluated for heart failure, and nuclear factor erythroid 2 –related factor 2 (NRF2) is one of them. NRF2 is a master transcription factor which is expressed in most of the tissues and exh...
Source: Journal of Cardiovascular Translational Research - November 25, 2020 Category: Cardiology Source Type: research
Isoproterenol-induced hypertrophy of neonatal cardiac myocytes and H9c2 cell is dependent on TRPC3-regulated CaV1.2 expression.
In this study, we aimed to examine the relationship between these two proteins and characterize their role in neonatal cardiomyocytes. We measured CaV1.2 expression in the hearts of wild-type (WT) and Trpc3-/- mice, and examined the effects of Trpc3 knockdown and overexpression in the rat cell line H9c2. We also compared the hypertrophic responses of neonatal cardiomyocytes cultured from Trpc3-/- mice to a representative hypertrophy-causing drug, isoproterenol (ISO), and measured the activity of nuclear factor of activated T cells 3 (NFAT3) in neonatal cardiomyocytes (NCMCs). We inhibited the L-type current with nifedipine...
Source: Cell Calcium - October 6, 2020 Category: Cytology Authors: Han JW, Kang C, Kim Y, Lee MG, Kim JY Tags: Cell Calcium Source Type: research
MFGE8 is down-regulated in cardiac fibrosis and attenuates endothelial-mesenchymal transition through Smad2/3-Snail signalling pathway.
In conclusion, our experiments indicate that MFGE8 might play a protective role in TGF-β1-induced EndMT and might be a potential therapeutic target for cardiac fibrosis.
PMID: 32945126 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - September 16, 2020 Category: Molecular Biology Authors: Wang B, Ge Z, Wu Y, Zha Y, Zhang X, Yan Y, Xie Y Tags: J Cell Mol Med Source Type: research
Endogenous CCN5 Participates in Angiotensin II/TGF- β1 Networking of Cardiac Fibrosis in High Angiotensin II-Induced Hypertensive Heart Failure
This study aimed to investigate the potential role of CCN5 in TGF-β1/Ang II networking-induced CF. Our clinical retrospective study demonstrated that serum CCN5 decreased in hypertensive patients, but significantly increased in hypertensive patients taking oral angiotensin-converting enzyme inhibitor (ACEI). A negative association was observed between CCN5 and Ang II in grade 2and 3 hypertensive patients receiving ACEI treatment. We further created an experimental model of high Ang II-induced hypertensive HF. CCN5 was downregulated in the spontaneously hypertensive rats (SHRs) and increased via the inhibition of Ang II pr...
Source: Frontiers in Pharmacology - September 2, 2020 Category: Drugs & Pharmacology Source Type: research
Kallistatin alleviates heart failure in rats by inhibiting myocardial inflammation and apoptosis via regulating sirt1.
CONCLUSIONS: KS reduces the inflammation and apoptosis of myocardial tissue in HF rats by promoting the expression of sirt1, thereby alleviating HF-induced myocardial injury.
PMID: 32572936 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - June 25, 2020 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research
Diabetes mellitus exacerbates post ‐myocardial infarction heart failure by reducing sarcolipin promoter methylation
ConclusionsDiabetes increases the vulnerability of STEMI patients to post ‐MI HF by down‐regulating SLN promoter methylation, which further regulates SERCA2a activity via increasing cardiac SLN expression.
Source: ESC Heart Failure - June 10, 2020 Category: Cardiology Authors: Zhongwei Liu,
Yong Zhang,
Chuan Qiu,
Haitao Zhu,
Shuo Pan,
Hao Jia,
Hongyan Kang,
Gongchang Guan,
Rutai Hui,
Ling Zhu,
Junkui Wang Tags: Original Research Article Source Type: research
CTRP15 derived from cardiac myocytes attenuates TGF β1-induced fibrotic response in cardiac fibroblasts
ConclusionCTRP15 exerts an anti-fibrotic effect on pressure overload-induced cardiac remodeling. The activation of IR/IRS-1/Akt pathway contributes to the anti-fibrotic effect of CTRP15 through targeting Smad3.
Source: Cardiovascular Drugs and Therapy - May 18, 2020 Category: Cardiology Source Type: research
From traditional pharmacological towards nucleic acid-based therapies for cardiovascular diseases
AbstractNucleic acid-based therapeutics are currently developed at large scale for prevention and management of cardiovascular diseases (CVDs), since: (i) genetic studies have highlighted novel therapeutic targets suggested to be causal for CVD; (ii) there is a substantial recent progress in delivery, efficacy, and safety of nucleic acid-based therapies; (iii) they enable effective modulation of therapeutic targets that cannot be sufficiently or optimally addressed using traditional small molecule drugs or antibodies. Nucleic acid-based therapeutics include (i) RNA-targeted therapeutics for gene silencing; (ii) microRNA-mo...
Source: European Heart Journal - April 29, 2020 Category: Cardiology Source Type: research
Danqi Pill Protects Against Heart Failure Post-Acute Myocardial Infarction via HIF-1 α/PGC-1α Mediated Glucose Metabolism Pathway
ConclusionsDQP exhibits the efficacy to improve myocardial glucose metabolism, mitochondrial oxidative phosphorylation and biogenesis by regulating HIF-1α/PGC-1α signaling pathway in HF post-AMI rats.
Source: Frontiers in Pharmacology - April 20, 2020 Category: Drugs & Pharmacology Source Type: research
Systemic Delivery of siRNA Specific for Silencing TLR4 Gene Expression Reduces Diabetic Cardiomyopathy in a Mouse Model of Streptozotocin-Induced Type 1 Diabetes
ConclusionOur study used siRNA to specifically silence TLR4 gene expression in the diabetic mouse heart in vivo and to investigate the role that TLR4 plays in diabetic cardiomyopathy. It is likely that silencing of the TLR4 gene through siRNA could prevent the development of diabetic cardiomyopathy.
Source: Diabetes Therapy - April 12, 2020 Category: Endocrinology Source Type: research
β-Arrestin2 regulates the rapid component of delayed rectifier K+ currents and cardiac action potential of guinea pig cardiomyocytes after adrenergic stimulation.
This study investigated the role of β-arrestin2 in the regulation of cardiac hERG/IKr potassium channel and AP during chronic adrenergic stimulation. Single left ventricular myocytes were isolated from guinea pig heart, and were transfected with adenovirus encoding β-arrestin2, or β-arrestin2 siRNA or an empty adenovirus. Cell cultures containing 10 nM isoproterenol, 1 nM phenylephrine or vehicle alone (control medium) were electro-physiologically examined after 48 h of incubation. Action potential duration at 50 and 90 % of repolarization (APD50 and APD90) were measured using whole-cell patch-clamp recording. Sustained...
Source: Cellular and Molecular Biology - December 29, 2019 Category: Molecular Biology Tags: Cell Mol Biol (Noisy-le-grand) Source Type: research
Hyperglycemia-induced cardiomyocyte death is mediated by lysosomal membrane injury and aberrant expression of cathepsin D.
Abstract
Hyperglycemia is an independent risk factor for diabetic heart failure. However, the mechanisms that mediate hyperglycemia-induced cardiac damage remain poorly understood. Previous studies have shown an association between lysosomal dysfunction and diabetic heart injury. The present study examined if mimicking hyperglycemia in cultured cardiomyocytes could induce lysosomal membrane permeabilization (LMP), leading to the release of lysosome enzymes and subsequent cell death. High glucose (HG) reduced the number of lysosomes with acidic pH as shown by a fluorescent pH indicator. Also, HG induced lysosomal m...
Source: Biochemical and Biophysical Research communications - December 16, 2019 Category: Biochemistry Authors: Kobayashi S, Zhao F, Kobayashi T, Hagiwara M, Kaminaris A, Li C, Cai F, Huang Y, Liang Q Tags: Biochem Biophys Res Commun Source Type: research
