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Condition: Heart Failure

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Total 253 results found since Jan 2013.

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

Neuropeptide Y mediates cardiac hypertrophy through microRNA-216b/FoxO4 signaling pathway.
Authors: Wang J, Hao D, Zeng L, Zhang Q, Huang W Abstract Cardiac hypertrophy (CH) is a major risk factor for heart failure accompanied by maladaptive cardiac remodeling. The role and potential mechanism of neuropeptide Y (NPY) in CH are still unclear. We will explore the role and the mechanism of NPY inactivation (NPY-I) in CH caused by pressure overload. Abdominal aortic constriction (AAC) was used to induce CH model in rats. NPY or angiotensin II (Ang II) was used to trigger CH model in vitro in neonatal rat ventricular myocytes (NRVMs). We found that NPY was increased in the heart and plasma of hypertrophic rat...
Source: International Journal of Medical Sciences - January 6, 2021 Category: Biomedical Science Tags: Int J Med Sci Source Type: research

Transmembrane tumor necrosis factor alpha attenuates pressure-overload cardiac hypertrophy via tumor necrosis factor receptor 2
by Kun Miao, Ling Zhou, Hongping Ba, Chenxi Li, Haiyan Gu, Bingjiao Yin, Jing Wang, Xiang-ping Yang, Zhuoya Li, Dao Wen Wang Tumor necrosis factor-alpha (TNF-α) plays an important pathogenic role in cardiac hypertrophy and heart failure (HF); however, anti-TNF is paradoxically negative in clinical trials and even worsens HF, indicating a possible protective role of TNF-α in HF. TNF-α exists in transmembrane (tmTNF-α ) and soluble (sTNF-α) forms. Herein, we found that TNF receptor 1 (TNFR1) knockout (KO) or knockdown (KD) by short hairpin RNA or small interfering RNA (siRNA) significantly alleviated cardiac hypertroph...
Source: PLoS Biology: Archived Table of Contents - December 3, 2020 Category: Biology Authors: Kun Miao 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

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

Haploid genetic screening identifies a novel regulator of BMPR2
Pulmonary arterial hypertension (PAH), is characterised by profound remodelling of small pulmonary arteries, leading to increased pulmonary arterial pressures and premature death by right heart failure. Heterozygous germ-line mutations in the bone morphogenetic protein type II receptor (BMPR2) cause ~70% of familial PAH and ~20% of idiopathic PAH cases. The majority of mutations lead to haploinsufficiency but crucially, regardless of the presence of mutation, lung BMPR2 expression is reduced in all forms of PAH. Therefore, restoration of BMPR2 levels is an important therapeutic target. We previously showed that BMPR2 ubiqu...
Source: European Respiratory Journal - October 28, 2020 Category: Respiratory Medicine Authors: Dunmore, B., Burr, S., Upton, P., Nathan, J., Morrell, N. Tags: Pulmonary hypertension Source Type: research

Novel Anti-inflammatory Effects of Canagliflozin Involving Hexokinase II in Lipopolysaccharide-Stimulated Human Coronary Artery Endothelial Cells
ConclusionCana conveys anti-inflammatory actions in LPS-treated HCAECs through 1) reductions in HKII and ERK1/2 phosphorylation and 2) AMPK activation. These data suggest a novel anti-inflammatory mechanism of Cana through HKII.
Source: Cardiovascular Drugs and Therapy - October 13, 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

Suppression of Netrin-1 attenuates angiotension II-induced cardiac remodeling through the PKC/MAPK signaling pathway.
CONCLUSIONS: Ang II produces cardiac hypertrophy, fibrosis, and apoptosis through the upregulation of Netrin-1 and the activation of the AT1R/PKCα/MAPK (JNK, P38) pathway. Suppression of Netrin-1 can relieve Ang II-induced cardiac remodeling via inhibition of the PKCα/MAPK (JNK and P38) signaling pathway. Thus, Netrin-1 may be a novel therapeutic target for Ang II-mediated cardiac remodeling. PMID: 32688140 [PubMed - as supplied by publisher]
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - July 16, 2020 Category: Drugs & Pharmacology Authors: Wu G, Wang Z, Shan P, Huang S, Lin S, Huang W, Huang Z Tags: Biomed Pharmacother Source Type: research

Glutamyl-Prolyl-tRNA Synthetase Regulates Proline-Rich Pro-fibrotic Protein Synthesis During Cardiac Fibrosis.
Conclusions: Our results indicate that EPRS preferentially controls translational activation of proline codon rich pro-fibrotic genes in cardiac fibroblasts and augments pathological cardiac remodeling. PMID: 32611237 [PubMed - as supplied by publisher]
Source: Circulation Research - June 30, 2020 Category: Cardiology Authors: Wu J, Subbaiah KCV, Xie LH, Jiang F, Khor ES, Mickelsen DM, Myers JR, Tang WW, Yao P Tags: Circ Res 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

The inotropic agent digitoxin strengthens desmosomal adhesion in cardiac myocytes in an ERK1/2-dependent manner
AbstractDesmosomal proteins are components of the intercalated disc and mediate cardiac myocyte adhesion. Enhancement of cardiac myocyte cohesion, referred to as “positive adhesiotropy”, was demonstrated to be a function of sympathetic signaling and to be relevant for a sufficient inotropic response. We used the inotropic agent digitoxin to investigate the link between inotropy and adhesiotropy. In contrast to wild-type hearts, digitoxin failed to enhanc e pulse pressure in perfused mice hearts lacking the desmosomal protein plakoglobin which was paralleled with abrogation of plaque thickening indicating that positive ...
Source: Basic Research in Cardiology - June 16, 2020 Category: Cardiology Source Type: research