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Specialty: Physiology
Condition: Heart Failure

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Total 15 results found since Jan 2013.

Reducing brain TACE activity improves neuroinflammation and cardiac function in heart failure rats
Tumor necrosis factor (TNF)-α converting enzyme (TACE) is a key metalloprotease mediating ectodomain shedding of a variety of inflammatory mediators, substrates, and growth factors. We previously reported that TACE-mediated production of TNF-α in the hypothalamic paraventricular nucleus (PVN) contributes to sympathetic excitation in heart failure (HF). Here, we sought to determine whether central interventions in TACE activity attenuate neuroinflammation and improve cardiac function in heart failure. Myocardial infarction-induced HF or sham-operated (SHAM) rats were treated with bilateral paraventricular nucleus microinj...
Source: Frontiers in Physiology - November 9, 2022 Category: Physiology Source Type: research

Protections of transcription factor BACH2 and natural product myricetin against pathological cardiac hypertrophy and dysfunction
This study aims to explore the role of BACH2, a member of the basic region leucine zipper transcription factor family, in cardiac hypertrophy and failure. Transverse aortic constriction surgery was operated to induce cardiac hypertrophy and failure in mice. BACH2 was overexpressed in mice through tail vein injection of AAV9-Bach2. Mice with systemic or cardiac-specific knockdown of Bach2 were adopted. Neonatal rat ventricular myocytes (NRVMs) were isolated and infected with lentivirus to overexpress Bach2 or transfected with siRNA to knock down Bach2. Our data showed that overexpression of BACH2 ameliorated TAC-induced car...
Source: Frontiers in Physiology - August 29, 2022 Category: Physiology Source Type: research

TMEM16A Plays an Insignificant Role in Myocardium Remodeling but May Promote Angiogenesis of Heart During Pressure-overload
Conclusion: TMEM16A contributes insignificantly in myocardium remodeling during pressure-overload. TMEM16A is a positive regulator of migration and angiogenesis under normal condition or simulated stress. TMEM16A may become a new target for upregulation of angiogenesis in ischemic disorders like ischemic heart disease.
Source: Frontiers in Physiology - May 31, 2022 Category: Physiology Source Type: research

CXCL10 is a novel anti ‐angiogenic factor downstream of p53 in cardiomyocytes
The conditioned media from p53-expressing cardiomyocytes decreased the tube formation of Rat Aortic Endothelial Cells. The blockade of CXCR3, a receptor of CXCL10, restored the angiogenic activity of the conditioned media from p53-expressing cardiomyocytes. AbstractTumor suppressor protein p53 plays crucial roles in the onset of heart failure. p53 activation results in cardiac dysfunction, at least partially by suppressing angiogenesis. Though p53  has been reported to reduce VEGF production by inhibiting hypoxia-inducible factor, the anti-angiogenic property of p53 remains to be fully elucidated in cardiomyocytes. To ex...
Source: Physiological Reports - May 11, 2022 Category: Physiology Authors: Tri Wahyuni, Shota Tanaka, Ryuta Igarashi, Yoshiaki Miyake, Ayaha Yamamoto, Shota Mori, Yusuke Kametani, Masashi Tomimatsu, Shota Suzuki, Kosei Yokota, Yoshiaki Okada, Makiko Maeda, Masanori Obana, Yasushi Fujio Tags: ORIGINAL ARTICLE 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

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

Salt-induced Na(+)/K(+)-ATPase- α/β expression involves soluble adenylyl cyclase in endothelial cells.
Salt-induced Na(+)/K(+)-ATPase-α/β expression involves soluble adenylyl cyclase in endothelial cells. Pflugers Arch. 2017 May 26;: Authors: Mewes M, Nedele J, Schelleckes K, Bondareva O, Lenders M, Kusche-Vihrog K, Schnittler HJ, Brand SM, Schmitz B, Brand E Abstract High dietary salt intake may lead to vascular stiffness, which predicts cardiovascular diseases such as heart failure, and myocardial and cerebral infarctions as well as renal impairment. The vascular endothelium is a primary target for deleterious salt effects leading to dysfunction and endothelial stiffness. We hypothesize that the Ca...
Source: Pflugers Archiv : European Journal of Physiology - May 26, 2017 Category: Physiology Authors: Mewes M, Nedele J, Schelleckes K, Bondareva O, Lenders M, Kusche-Vihrog K, Schnittler HJ, Brand SM, Schmitz B, Brand E Tags: Pflugers Arch Source Type: research

Contribution of two pore potassium channels to cardiac ventricular action potential revealed using human iPSC-derived cardiomyocytes.
Abstract Two pore potassium channels (K2p) have been described in modulating background conductance as leak channels in different physiological systems. In the heart, the expression of K2p channels is heterogeneous with equivocation regarding their functional role. Our objective was to determine the K2p expression profile and their physiological and pathophysiological contribution to cardiac electrophysiology. Induced pluripotent stem cells (iPSC) cells generated from humans were differentiated into cardiomyocytes (iPSC-CM). mRNA was isolated from these cells, commercial iPSC-CM (iCells®), control human heart ven...
Source: American Journal of Physiology. Heart and Circulatory Physiology - March 24, 2017 Category: Physiology Authors: Chai S, Wan X, Nassal DM, Liu H, Moravec CS, Ramirez-Navarro A, Deschenes I Tags: Am J Physiol Heart Circ Physiol Source Type: research

Endostatin is protective against monocrotaline-induced right heart disease through the inhibition of T-type Ca(2+) channel.
Abstract Endostatin (ES), a C-terminal fragment of collagen XVIIIα1, has a potent anti-angiogenic effect. ES prevents tumor proliferation through inhibiting T-type Ca(2+) channel. T-type Ca(2+) channel is re-expressed during heart diseases including monocrotaline (MCT)-induced right heart failure. The present study aimed to clarify the effects of ES on T-type Ca(2+) channel and pathogenesis of MCT-induced right ventricular disease. MCT or saline was injected intraperitoneally to rats. After cardiomyocytes were isolated from right ventricles (RVs), T-type Ca(2+) channel current (I CaT) was measured by a patch-clam...
Source: Pflugers Archiv : European Journal of Physiology - March 28, 2016 Category: Physiology Authors: Imoto K, Kumatani S, Okada M, Yamawaki H Tags: Pflugers Arch Source Type: research

Tumor necrosis factor-α impairs adiponectin signalling, mitochondrial biogenesis and myogenesis in primary human myotubes cultures.
CONCLUSION: Major features of adiponectin resistance are retained in primary cultures from the skeletal muscle of HFrEF patients. In addition, our results suggest that an increased inflammatory constitution contributes to adiponectin resistance and confers alterations in skeletal muscle differentiation, growth and function. PMID: 26921438 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Heart and Circulatory Physiology - February 26, 2016 Category: Physiology Authors: Sente T, Van Berendoncks AM, Fransen E, Vrints CJ, Hoymans VY Tags: Am J Physiol Heart Circ Physiol Source Type: research

ERK1/2 MAPK Signaling in Hypothalamic Paraventricular Nucleus Contributes to Sympathetic Excitation in Rats with Heart Failure after Myocardial Infarction.
Abstract Brain mitogen-activated protein kinase (MAPK) signaling pathways are activated in heart failure (HF) induced by myocardial infarction and contribute to augmented sympathetic nerve activity. We tested whether silencing brain extracellular signal-regulated kinases 1 and 2 (ERK1/2, also known as p44/42 MAPK) in the hypothalamic paraventricular nucleus (PVN), a forebrain source of presympathetic neurons, would reduce the upregulation of sympatho-excitatory mediators in the PVN and the augmented sympathetic nerve activity in rats with HF. Sprague-Dawley rats underwent left anterior descending coronary artery l...
Source: American Journal of Physiology. Heart and Circulatory Physiology - January 22, 2016 Category: Physiology Authors: Yu Y, Wei SG, Zhang ZH, Weiss RM, Felder RB Tags: Am J Physiol Heart Circ Physiol Source Type: research

Pro-B-type natriuretic peptide is cleaved intracellularly: impact of distance between O-glycosylation and cleavage sites
We examined the molecular forms of secreted and intracellular BNP in atrial and ventricular myocytes; levels of corin and furin mRNA in atrial and ventricular myocytes; the effect their knockdown on proBNP processing; plasma molecular forms of BNP from rats and humans with and without heart failure; and the impact of the distance between the glycosylation and cleavage sites in wild-type and mutant human proBNP, expressed in rat myocytes transfected with lentiviral vectors. BNP was the major molecular form secreted by atrial and ventricular myocytes. Transfection of furin siRNA reduced proBNP processing in both atrial and v...
Source: AJP: Regulatory, Integrative and Comparative Physiology - September 15, 2015 Category: Physiology Authors: Nishikimi, T., Nakagawa, Y., Minamino, N., Ikeda, M., Tabei, K., Fujishima, A., Takayama, K., Akimoto, K., Yamada, C., Nakao, K., Minami, T., Kuwabara, Y., Kinoshita, H., Tsutamoto, T., Ishimitsu, T., Kangawa, K., Kuwahara, K., Nakao, K. Tags: Hormones, Reproduction and Development Source Type: research

Pro-B-type natriuretic peptide is cleaved intracellularly: impact of distance between O-glycosylation and cleavage sites.
We examined the molecular forms of secreted and intracellular BNP in atrial and ventricular myocytes; levels of corin and furin mRNA in atrial and ventricular myocytes; the effect their knockdown on proBNP processing; plasma molecular forms of BNP from rats and humans with and without heart failure; and the impact of the distance between the glycosylation and cleavage sites in wild-type and mutant human proBNP expressed in rat myocytes transfected with lentiviral vectors. BNP was the major molecular form secreted by atrial and ventricular myocytes. Transfection of furin siRNA reduced proBNP processing in both atrial and ve...
Source: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology - July 1, 2015 Category: Physiology Authors: Nishikimi T, Nakagawa Y, Minamino N, Ikeda M, Tabei K, Fujishima A, Takayama K, Akimoto K, Yamada C, Nakao K, Minami T, Kuwabara Y, Kinoshita H, Tsutamoto T, Ishimitsu T, Kangawa K, Kuwahara K, Nakao K Tags: Am J Physiol Regul Integr Comp Physiol Source Type: research

Contribution of sodium channel neuronal isoform Nav 1.1 to late sodium current in ventricular myocytes from failing hearts.
In conclusion, we have discovered an Nav 1.1-originated INaL component in dog heart ventricular cells. This component is physiologically relevant to controlling AP shape and duration, as well as to cell Ca(2+) dynamics. PMID: 25772296 [PubMed - in process]
Source: The Journal of Physiology - March 15, 2015 Category: Physiology Authors: Mishra S, Reznikov V, Maltsev VA, Undrovinas NA, Sabbah HN, Undrovinas A Tags: J Physiol Source Type: research

Contribution of neuronal isoform Nav1.1 to late sodium current in ventricular myocytes from failing hearts.
In conclusion, we have discovered Nav1.1-originated INaL component in dog heart ventricular cells. This component is physiologically relevant to control AP shape and duration, as well as to cell Ca(2+) dynamics. This article is protected by copyright. All rights reserved. PMID: 25326451 [PubMed - as supplied by publisher]
Source: The Journal of Physiology - October 17, 2014 Category: Physiology Authors: Mishra S, Reznikov V, Maltsev VA, Undrovinas NA, Sabbah HN, Undrovinas A Tags: J Physiol Source Type: research