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Condition: Heart Failure

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Total 253 results found since Jan 2013.

Epoxyeicosatrienoic acid prevents maladaptive remodeling in pressure overload by targeting calcineurin/NFAT and Smad-7.
CONCLUSIONS: EET has synergistic actions on cardiomyocytes and cardiac fibroblasts, preventing cardiac hypertrophy through inhibition of Ca2+-mediated calcineurin/NFATc3 signaling cascades, and ameliorating myocardial fibrosis dependent on Smad-7. This work further extends the potential mechanisms of EET, providing a novel therapeutic approach for the treatment of pathological remodeling and heart failure. PMID: 31734152 [PubMed - as supplied by publisher]
Source: Experimental Cell Research - November 13, 2019 Category: Cytology Authors: Li X, Chu G, Zhu F, Zheng Z, Wang X, Zhang G, Wang F Tags: Exp Cell Res Source Type: research

Downregulation of TRAP1 aggravates injury of H9c2 cardiomyocytes in a hyperglycemic state.
In conclusion, the present findings suggested that the decrease in cardiomyocyte TRAP1 expression under high glucose conditions was associated with myocardial injury. It was hypothesized that TRAP1 may have a protective role on cardiomyocytes under high glucose surroundings. PMID: 31572516 [PubMed]
Source: Experimental and Therapeutic Medicine - October 2, 2019 Category: General Medicine Tags: Exp Ther Med Source Type: research

Adenine decreases hypertrophic effects through interleukin-18 receptor.
In this study, IL-18 induced cardiomyoblast hypertrophy through IL-18R upregulation, which was found to be related to p38 MAPK and PI3 kinase signaling. Adenine, but not AuNPs, showed antihypertrophic effects possibly because of decreased levels of signaling. PMID: 31535629 [PubMed - in process]
Source: The Chinese Journal of Physiology - September 20, 2019 Category: Physiology Tags: Chin J Physiol Source Type: research

Upregulation of miR-93 and inhibition of LIMK1 improve ventricular remodeling and alleviate cardiac dysfunction in rats with chronic heart failure by inhibiting RhoA/ROCK signaling pathway activation.
CONCLUSION: Our study provides evidence that upregulated miR-93 and downregulated LIMK1 improve ventricular remodeling and reduce cardiac dysfunction in CHF rats by inhibiting RhoA/ROCK signaling pathway activation. METHODS: First, rat models of CHF were established by aortic coarctation, and the rats were injected with miR-93 mimics, LIMK1-siRNA or overexpressed-LIMK1. Then expression of miR-93, LIMK1, RhoA, and ROCK1 expression in myocardial tissues were detected, after which indices of cardiac ultrasound, hemodynamics, and oxidative stress, inflammatory factors, apoptosis-related indicators were detected via a seri...
Source: Aging - September 19, 2019 Category: Biomedical Science Authors: Su Q, Zhang P, Yu D, Wu Z, Li D, Shen F, Liao P, Yin G Tags: Aging (Albany NY) Source Type: research

MicroRNA-92b-3p suppresses angiotensin II-induced cardiomyocyte hypertrophy via targeting HAND2
In this study, we want to investigate the role of microRNA-92b-3p (miR-92b-3p) in cardiomyocyte hypertrophy and the mechanisms involved.Materials and methodsNeonatal mouse ventricular cells (NMVCs) were isolated from the hearts of 1–3-d-old newborn C57BL6 mice. The isolated NMVCs were induced hypertrophic phenotype by Angiotensin-II (Ang-II) and the cell size was examined by FITC-phalloidin staining assay. The expression of miR-92b-3p was determined by quantitative real-time PCR (qRT-qPCR). MRNA and protein level of β-MHC, ACTA1 and HAND2 in NMVCs transfected with miR-92b-3p mimic and inhibition were assessed by RT-qPCR...
Source: Life Sciences - July 6, 2019 Category: Biology Source Type: research

Role of TLR4/NADPH oxidase 4 pathway in promoting cell death through autophagy and ferroptosis during heart failure.
Abstract Loss of myocytes caused by cell death plays a key role during heart failure (HF). Activated autophagy and increased ferroptosis have been observed in HF and proved to promote its progression. However, the underlying mechanisms remain unclear. Here, results from integrated bioinformatical analysis showed TLR4 and NADPH oxidase 4 (NOX4) were included in up-regulated differentially expressed genes (DEGs), and had an interaction between each other inferred by the DEGs-associated protein-protein interaction (PPI) network. To explore the role of TLR4-NOX4 in autophagy and ferroptosis, knock-down of TLR4 and NOX...
Source: Biochemical and Biophysical Research communications - June 9, 2019 Category: Biochemistry Authors: Chen X, Xu S, Zhao C, Liu B Tags: Biochem Biophys Res Commun Source Type: research

Endothelial Foxp1 Regulates Pathological Cardiac Remodeling Through TGF- β1-Endothelin-1 Signal Pathway.
CONCLUSIONS: EC-Foxp1 regulates the TGF-β1-ET-1 pathway to control pathological cardiac fibrosis and hypertrophy, resulting in cardiac dysfunction. Therefore, targeting the EC-Foxp1-TGF-β1-ET-1 pathway might provide a future novel therapy for heart failure. PMID: 31177814 [PubMed - as supplied by publisher]
Source: Circulation - June 9, 2019 Category: Cardiology Authors: Liu J, Zhuang T, Pi J, Chen X, Zhang Q, Li Y, Wang H, Shen Y, Tomlinson B, Chan P, Yu Z, Cheng Y, Zheng X, Reilly M, Morrisey E, Zhang L, Liu Z, Zhang Y Tags: Circulation Source Type: research

miRNA-218 Targets Lipin-1 and Glucose Transporter Type 4 Genes in 3T3-L1 Cells Treated With Lopinavir/Ritonavir
Conclusion: 3T3-L1 cells, treated with LPV/RTV, show altered lipid content due to increased miRNA-218 levels, which affects lipin-1 mRNA. Moreover, increased miRNA-218 levels were inversely correlated with changes in GLUT-4 expression, which suggests a role for miRNA-218 in mediating the insulin resistance consequent to cART. Introduction Metabolic syndrome is a serious consequence of combined Antiretroviral Therapy (cART). HIV-associated metabolic syndrome is often accompanied by lipodystrophy (LS), the redistribution of body fat with loss of subcutaneous adipose tissue in face, limbs and buttocks, concomitant wit...
Source: Frontiers in Pharmacology - April 29, 2019 Category: Drugs & Pharmacology Source Type: research

FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/ β-Catenin Pathway in a Murine Model of Lupus Nephritis
In this study, we therefore examined whether FKN could stimulate the process of EMT, NF-kB, TGFβ, CCL22, F4/80, inflammation, and tubulointerstitial fibrosis in a murine model of LN. We also determined whether FKN was involved in the EMT process of Wnt/β-catenin-expressing HK-2 cells. Mechanistically, we ascertained, for the first time, whether FKN up-regulated EMT-related gene signatures (e.g., vimentin, α-SMA), and hence, renal tubulointerstitial fibrogenesis, and the role of the Wnt/β-catenin signaling pathway in this process. Materials and Methods Cell Culture, Stable Infection, and Gr...
Source: Frontiers in Immunology - April 29, 2019 Category: Allergy & Immunology Source Type: research

Cardiotonic steroid ouabain stimulates steroidogenesis in Leydig cells via the α3 isoform of the sodium pump
Publication date: Available online 28 April 2019Source: The Journal of Steroid Biochemistry and Molecular BiologyAuthor(s): Neha Upmanyu, Raimund Dietze, Ahmed Bulldan, Georgios Scheiner-BobisAbstractCardiotonic steroids such as ouabain are potent inhibitors of the sodium pump and have been widely used for centuries in the treatment of congestive heart failure. In recent decades, however, they have also been identified as hormone-like molecules that trigger signaling cascades of physiological relevance by using the various sodium pump α subunit isoforms as receptors. The murine Leydig cell line MLTC-1 expresses both the u...
Source: The Journal of Steroid Biochemistry and Molecular Biology - April 29, 2019 Category: Biochemistry Source Type: research

FGF21 as Modulator of Metabolism in Health and Disease
In conclusion, FGF21 belongs to a promising class of cytokines that are induced in response to stress and that can be used as a drug, drug target, or through a biomarker, depending on the physio-pathological context. All these findings will become clear when FGF21 will be used as a therapeutic molecule, exploiting the beneficial effects of FGF21 for treating metabolic disease or when it will be blocked to ameliorate disease progression and the onset of disease. Author Contributions CT and MS wrote the manuscript. VR contributed to the discussion. Funding This work was supported from the AFM-Telethon (19524), Italian Mi...
Source: Frontiers in Physiology - April 16, 2019 Category: Physiology Source Type: research

Loss of reticulocalbin 2 lowers blood pressure and restrains angiotensin II-induced hypertension in vivo.
Abstract Hypertension affects over one billion people worldwide and increases risk for heart failure, stroke and chronic kidney disease. Despite high prevalence and devastating impact, its etiology still remains poorly understood for most hypertensive cases. Rcn2, encoding reticulocalbin 2, is a candidate gene for atherosclerosis we previously demonstrated in mice. Here we identified Rcn2 as a novel regulator of blood pressure in mice. Rcn2 was dramatically upregulated in arteries undergoing structural remodeling. Deletion of Rcn2 lowered basal blood pressure and attenuated angiotensin II-induced hypertension in C...
Source: Am J Physiol Renal P... - April 2, 2019 Category: Urology & Nephrology Authors: Li J, Cechova S, Wang L, Isakson BE, Le T, Shi W Tags: Am J Physiol Renal Physiol Source Type: research

The Long Non-Coding RNA CPR Regulates Cardiomyocyte Proliferation and Cardiac Repair.
CONCLUSIONS: Together, our findings identified that CPR is a suppressor of cardiomyocyte proliferation, and it indicates that lncRNA(s) take parts in the regulation of cardiomyocyte proliferation and cardiac repair. Our study provides an lncRNA-based therapeutic strategy for effective cardiac repair and regeneration. PMID: 30832495 [PubMed - as supplied by publisher]
Source: Circulation - March 4, 2019 Category: Cardiology Authors: Ponnusamy M, Liu F, Zhang YH, Li RB, Zhai M, Liu F, Zhou LY, Liu CY, Yan KW, Dong YH, Wang M, Qian LL, Shan C, Xu S, Wang Q, Zhang YH, Li PF, Zhang J, Wang K Tags: Circulation Source Type: research

Activation of T Lymphocytes as a Novel Mechanism in Beta1-Adrenergic Receptor Autoantibody-Induced Cardiac Remodeling
ConclusionsCollectively, we demonstrate that β1-AAmAb-induced cardiac remodeling via mediating T lymphocyte disorder and releasing a variety of IL-6.
Source: Cardiovascular Drugs and Therapy - February 12, 2019 Category: Cardiology Source Type: research

Adeno-associated virus 9-mediated RNA interference targeting SOCS3 alleviates diastolic heart failure in rats.
CONCLUSIONS: SOCS3 gene silencing by AAV9-SOCS3 siRNA administration in a DHF rat model significantly reduced myocardial fibrosis and the inflammatory response and improved heart function. Therefore, this treatment is a potential therapeutic method for treating DHF. PMID: 30763670 [PubMed - as supplied by publisher]
Source: Gene - February 11, 2019 Category: Genetics & Stem Cells Authors: Gao J, Guo Y, Chen Y, Zhou J, Liu Y, Su P Tags: Gene Source Type: research