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Condition: Heart Failure

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Total 253 results found since Jan 2013.

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

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

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

Anti-inflammatory effects of higenamine (Hig) on LPS-activated mouse microglia (BV2) through NF- κB and Nrf2/HO-1 signaling pathways.
Anti-inflammatory effects of higenamine (Hig) on LPS-activated mouse microglia (BV2) through NF-κB and Nrf2/HO-1 signaling pathways. Int Immunopharmacol. 2020 Jun 11;85:106629 Authors: Yang S, Chu S, Ai Q, Zhang Z, Gao Y, Lin M, Liu Y, Hu Y, Li X, Peng Y, Pan Y, He Q, Chen N Abstract Microglia are the most widely equipped protective cells in the brain and play a pivotal role in the development of neurological diseases. Inflammatory response and oxidative stress are critical risk factors in the activation of microglia which may cause various neurological diseases. Higenamine (Hig), a plant-based alkal...
Source: International Immunopharmacology - June 10, 2020 Category: Allergy & Immunology Authors: Yang S, Chu S, Ai Q, Zhang Z, Gao Y, Lin M, Liu Y, Hu Y, Li X, Peng Y, Pan Y, He Q, Chen N Tags: Int Immunopharmacol 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

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

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

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

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

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

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

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

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

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

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