scholarly journals Statin-Induced Nitric Oxide Signaling: Mechanisms and Therapeutic Implications

2019 ◽  
Vol 8 (12) ◽  
pp. 2051 ◽  
Author(s):  
Armita Mahdavi Gorabi ◽  
Nasim Kiaie ◽  
Saeideh Hajighasemi ◽  
Maciej Banach ◽  
Peter E. Penson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Blood Pressure ◽  
Atherosclerotic Plaques ◽  
Therapeutic Effects ◽  
Therapeutic Implications ◽  
Nitric Oxide Signaling ◽  
Beneficial Effects ◽  
Signaling Mechanisms ◽  
Neurological Injuries

In addition to their cholesterol-lowering effects, statins are associated with pleiotropic effects including improvements in heart failure (HF), reduced blood pressure, prevention of the rupture of atherosclerotic plaques and improved angiogenesis. In addition to these cardiovascular benefits, statins have been implicated in the treatment of neurological injuries, cancer, sepsis, and cirrhosis. These cholesterol-independent beneficial effects of statins are predominantly mediated through signaling pathways leading to increased production and bioavailability of nitric oxide (NO). In this review, the mechanistic pathways and therapeutic effects of statin-mediated elevations of NO are described and discussed.

Abstract P388: Extra-cardiac BCAA Catabolism Lowers Blood Pressure And Protects From Heart Failure

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Danielle Murashige ◽  
Cholsoon Jang ◽  
Michael Neinast ◽  
Michael Levin ◽  
Jae Woo Jung ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Blood Pressure ◽  
Mendelian Randomization ◽  
Multiple Models ◽  
Direct Effects ◽  
Heavy Isotope ◽  
Branched Chain Amino Acid ◽  
Branched Chain

Pharmacologic activation of branched chain amino acid (BCAA) catabolism is protective in numerous models of heart failure (HF). How this protection occurs has remained unclear, although a causative block in cardiac BCAA oxidation has been proposed. We use here in vivo heavy isotope infusion studies to show that cardiac preference for BCAA oxidation increases, rather than decreases, in multiple models of HF. We use various genetic models to show that cardiac-specific activation of BCAA oxidation does not protect from HF, even though systemic activation of BCAA oxidation does. Lowering plasma and cardiac BCAAs by genetic means is also not sufficient to confer protection comparable to that conferred by pharmacologic activation of BCAA oxidation, suggesting alternative mechanisms of protection. Surprisingly, telemetry and invasive hemodynamic studies showed that pharmacological activation of BCAA catabolism lowers blood pressure, a well-established cardioprotective mechanism. The effects on blood pressure occurred independently of nitric oxide (NO), and reflected a vascular resistance to adrenergic constriction. Finally, mendelian randomization studies revealed that elevations in plasma BCAAs portend higher blood pressure in large human cohorts. Together, these data indicate that activation of BCAA oxidation lowers blood pressure and protects from heart failure independently of any direct effects on the heart itself.

scholarly journals Potential mechanisms for the effects of far-infrared on the cardiovascular system – a review

VASA ◽  
2019 ◽  
Vol 48 (4) ◽  
pp. 303-312 ◽  
Author(s):  
Richard Shemilt ◽  
Hala Bagabir ◽  
Chim Lang ◽  
Faisel Khan
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular System ◽  
Animal Studies ◽  
Cardiovascular Health ◽  
Far Infrared ◽  
Therapeutic Effects ◽  
Beneficial Effects ◽  
Wide Range ◽  
Shock Proteins ◽  
Endothelial Nitric Oxide

Abstract. Far-infrared (FIR) is a form of thermal radiation, which may have beneficial effects on cardiovascular health. Clinical studies suggest that FIR irradiation may have therapeutic effects in heart failure, myocardial ischaemia and may improve flow and survival of arteriovenous fistula. Animal studies have suggested a wide range of potential mechanisms involving endothelial nitric oxide synthase and nitric oxide bioavailability, oxidative stress, heat shock proteins and endothelial precursor cells. However, the exact cellular and molecular mechanism of FIR on the cardiovascular system remains elusive. The purpose of this review is to discuss the current literature, focusing on mechanistic studies involving the cardiovascular system, and with a view to highlighting areas for future investigation.

scholarly journals TaiChi and Qigong for Depressive Symptoms in Patients with Chronic Heart Failure: A Systematic Review with Meta-Analysis

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Wei Jiang ◽  
Shaojun Liao ◽  
Xiankun Chen ◽  
Cecilia Stålsby Lundborg ◽  
Gaetano Marrone ◽  
...  
Keyword(s):  
Heart Failure ◽  
Systematic Review ◽  
Depressive Symptoms ◽  
Meta Analysis ◽  
Controlled Trials ◽  
Therapeutic Effects ◽  
Cochrane Central Register ◽  
China National Knowledge Infrastructure ◽  
Beneficial Effects ◽  
Meta Analyses

Background. Depression is a debilitating comorbidity of heart failure (HF) that needs assessment and management. Along with mind-body exercise to deal with HF with depression, the use of TaiChi and/or Qigong practices (TQPs) has increased. Therefore, this systematic review assesses the effects of TQPs on depression among patients with HF. Methods. Randomized controlled trials (RCTs) that examined the effect of TQPs on depression in patients with HF were searched by five databases (PubMed, Cochrane Central Register of Controlled Trials (CENTRAL), EMBASE, CINAHL, and China National Knowledge Infrastructure (CNKI)). With standardized mean difference (SMD) and 95% confidence intervals (95% CI), random-effects meta-analyses of the effect of TQPs on depressive symptoms were performed. Results. Of eight included RCTs, seven (481 patients) provided data for the meta-analysis. The pooling revealed that TQPs contribute to depression remission in HF (SMD −0.66; 95% CI −0.98 to −0.33, P < 0.0001 ; I2 = 64%). Its antidepressive effect was not influenced by intervention duration or exercise setting, but rather by ejection fraction subtype, depressive severity, and depression instruments. The beneficial effects were preserved when the study with the largest effect was removed. Conclusion. This study suggests that TQPs might be a good strategy for alleviating depressive symptoms in patients with HF. And rigorous-design RCTs, which focus on the identified research gaps, are needed to further establish the therapeutic effects of TQPs for depression in HF.

scholarly journals Nitric Oxide Signaling in Plants

Plants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1550
Author(s):  
John T. Hancock
Keyword(s):  
Nitric Oxide ◽  
Cell Signaling ◽  
Developmental Stages ◽  
Physiological Responses ◽  
Post Translational Modifications ◽  
Nitric Oxide Signaling ◽  
Signaling Mechanisms ◽  
Oxide Synthase ◽  
Signaling Components ◽  
Aperture Closure

Nitric oxide (NO) is an integral part of cell signaling mechanisms in animals and plants. In plants, its enzymatic generation is still controversial. Evidence points to nitrate reductase being important, but the presence of a nitric oxide synthase-like enzyme is still contested. Regardless, NO has been shown to mediate many developmental stages in plants, and to be involved in a range of physiological responses, from stress management to stomatal aperture closure. Downstream from its generation are alterations of the actions of many cell signaling components, with post-translational modifications of proteins often being key. Here, a collection of papers embraces the differing aspects of NO metabolism in plants.

scholarly journals Author Correction: A rare genetic variant of BPIFB4 predisposes to high blood pressure via impairment of nitric oxide signaling

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Carmine Vecchione ◽  
Francesco Villa ◽  
Albino Carrizzo ◽  
Chiara Carmela Spinelli ◽  
Antonio Damato ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
High Blood Pressure ◽  
Genetic Variant ◽  
Rare Genetic Variant ◽  
Nitric Oxide Signaling

scholarly journals A rare genetic variant of BPIFB4 predisposes to high blood pressure via impairment of nitric oxide signaling

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Carmine Vecchione ◽  
Francesco Villa ◽  
Albino Carrizzo ◽  
Chiara Carmela Spinelli ◽  
Antonio Damato ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
High Blood Pressure ◽  
Genetic Variant ◽  
Rare Genetic Variant ◽  
Nitric Oxide Signaling

Abstract 16763: Mechanical Circulatory Support Promotes Myocardial Nitric Oxide Signaling in Heart Failure Patients

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
David J Polhemus ◽  
Ya-Xiong Tao ◽  
Steven C Koenig ◽  
Sumanth D Prabhu ◽  
David Lefer
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Soluble Guanylyl Cyclase ◽  
Left Ventricular ◽  
Circulatory Support ◽  
Nitric Oxide Signaling ◽  
Protein Levels ◽  
Patients With Heart Failure ◽  
No Bioavailability ◽  
Preclinical Animal Models

Introduction: The integrity of the cardiovascular system is dependent on the continuous generation of nitric oxide (NO). Reduction in NO bioavailability is central to the development of cardiovascular disorders and patients with heart failure (HF) exhibit blunted endothelium-dependent flow-mediated dilation in indicating diminished NO release. We have previously reported that patients with heart failure have marked reductions in circulating NO metabolites and that NO-based therapies significantly reverse left ventricular (LV) dysfunction in preclinical animal models of HF. Methods: Plasma and left ventricular (LV) tissue were collected in HF patients (n=10) at the time of left ventricular assist device (LVAD) implantation. Plasma and LV tissue were again collected in the same 10 patients at the time of cardiac transplantation. Plasma and cardiac nitrite concentrations were determined by ion chromatography methods and nitrosylated protein (RXNO) levels were measured by chemiluminescence detection. Cyclic guanosine 5’-monophosphate (cGMP) was analyzed using radioimmunoassay technique. Results: Results: Following LVAD implantation, RXNO (NO-bound protein) levels were significantly elevated in both circulation and in the LV (10.2 nM vs. 33.3 nM, p < 0.05). Downstream NO signaling activates soluble guanylyl cyclase to form cGMP. Interestingly, LV cGMP levels were significantly augmented post-LVAD implantation (p<0.01). In contrast, plasma and cardiac nitrite (NO2) levels remained unchanged. Conclusions: These data strongly suggest that cardiovascular remodeling accompanying LVAD implantation promotes endothelial nitric oxide synthase (eNOS) function and increases NO bioavailability and signaling.

scholarly journals EET intervention on Wnt1, NOV, and HO-1 signaling prevents obesity-induced cardiomyopathy in obese mice

2017 ◽  
Vol 313 (2) ◽  
pp. H368-H380 ◽  
Author(s):  
Jian Cao ◽  
Shailendra P. Singh ◽  
John A. McClung ◽  
Gregory Joseph ◽  
Luca Vanella ◽  
...  
Keyword(s):  
Heart Failure ◽  
Vascular Function ◽  
Fasting Blood Glucose ◽  
Peroxisome Proliferator ◽  
Epoxyeicosatrienoic Acid ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cardiac Tissues ◽  
Beneficial Effects ◽  
Signaling Mechanisms ◽  
Mitochondrial Integrity

We have previously reported that epoxyeicosatrienoic acid (EET) has multiple beneficial effects on vascular function; in addition to its antiapoptotic action, it increases insulin sensitivity and inhibits inflammation. To uncover the signaling mechanisms by which EET reduces cardiomyopathy, we hypothesized that EET infusion might ameliorate obesity-induced cardiomyopathy by improving heme oxygenase (HO)-1, Wnt1, thermogenic gene levels, and mitochondrial integrity in cardiac tissues and improved pericardial fat phenotype. EET reduced levels of fasting blood glucose and proinflammatory adipokines, including nephroblastoma overexpressed (NOV) signaling, while increasing echocardiographic fractional shortening and O2 consumption. Of interest, we also noted a marked improvement in mitochondrial integrity, thermogenic genes, and Wnt 1 and HO-1 signaling mechanisms. Knockout of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) in EET-treated mice resulted in a reversal of these beneficial effects including a decrease in myocardial Wnt1 and HO-1 expression and an increase in NOV. To further elucidate the effects of EET on pericardial adipose tissues, we observed EET treatment increases in adiponectin, PGC-1α, phospho-AMP-activated protein kinase, insulin receptor phosphorylation, and thermogenic genes, resulting in a “browning” pericardial adipose phenotype under high-fat diets. Collectively, these experiments demonstrate that an EET agonist increased Wnt1 and HO-1 signaling while decreasing NOV pathways and the progression of cardiomyopathy. Furthermore, this report presents a portal into potential therapeutic approaches for the treatment of heart failure and metabolic syndrome. NEW & NOTEWORTHY The mechanism by which EET acts on obesity-induced cardiomyopathy is unknown. Here, we describe a previously unrecognized function of EET infusion that inhibits nephroblastoma overexpressed (NOV) levels and activates Wnt1, hence identifying NOV inhibition and enhanced Wnt1 expression as novel pharmacological targets for the prevention and treatment of cardiomyopathy and heart failure. Listen to this article's corresponding podcast at http://ajpheart.physiology.org/content/early/2017/05/31/ajpheart.00093.2017 .

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