Cytokines and Heart Failure: Pathophysiological Roles and Therapeutic Implications

Heart Failure ◽  
2000 ◽  
pp. 35-45
Author(s):  
Akira Matsumori
Keyword(s):  
Heart Failure ◽  
Therapeutic Implications

Conivaptan: Potential Therapeutic Implications in Heart Failure

2008 ◽  
Vol 3 (2) ◽  
pp. 137-140 ◽  
Author(s):  
Stephen Chen ◽  
Zuheir Abrahams ◽  
George Sokos ◽  
Wilfried Mullens ◽  
Robert Hobbs ◽  
...  
Keyword(s):  
Heart Failure ◽  
Therapeutic Implications

Adrenergic and muscarinic receptor regulation and therapeutic implications in heart failure

1996 ◽  
Vol 157 (1-2) ◽  
Author(s):  
Wilhelm Schmitz ◽  
Peter Boknik ◽  
Bettina Linck ◽  
FrankU. M�ller
Keyword(s):  
Heart Failure ◽  
Muscarinic Receptor ◽  
Receptor Regulation ◽  
Therapeutic Implications

scholarly journals Hyperuricemia and the Risk of Heart Failure: Pathophysiology and Therapeutic Implications

2021 ◽  
Vol 12 ◽  
Author(s):  
Ke Si ◽  
Chijing Wei ◽  
Lili Xu ◽  
Yue Zhou ◽  
Wenshan Lv ◽  
...  
Keyword(s):  
Heart Failure ◽  
Vascular Inflammation ◽  
Cardiovascular Effects ◽  
Daily Practice ◽  
Left Ventricular ◽  
Therapeutic Interventions ◽  
Current Evidence ◽  
Free Oxygen Radical ◽  
Positive Role ◽  
Therapeutic Implications

The association between hyperuricemia and cardiovascular disease (CVD) has been reported and studied in the past two decades. Xanthine oxidase (XO) induced uric acid (UA) serves as a risk factor and has the independent prognostic and functional impact of heart failure (HF), but whether it plays a positive role in the pathogenesis of HF has remained unclear. Growing evidence suggest the up-regulated XO avtivity and increased production of free oxygen radical (ROS) correspondingly are the core pathogenesis of HF with hyperuricemia, which results in a whole cluster of pathophysiologic cardiovascular effects such as oxidative stress, endothelial dysfunction, vascular inflammation, left ventricular (LV) dysfunction as well as insulin resistance (IR). The use of XO inhibition represents a promising therapeutic choice in patients with HF due to its dual effect of lowering serum UA levels as well as reducing ROS production. This review will discuss the pathophysiologic mechanisms of hyperuricemia with HF, the targeted therapeutic interventions of UA lowering therapies (ULT) with XO inhibition and mechanism underlying beneficial effects of ULT. In addition, the review also summarizes current evidence on the role of ULT in HF and compares CV risk between allopurinol and febuxostat for practical and clinical purposes. Guidelines and implementation of CV risk management in daily practice will be discussed as well.

Abstract 372: MicroRNA-9 Inhibits Hyperglycemia-induced Cardiac Pyroptosis by Targeting ELAVL1

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Prince Jeyabal ◽  
Rajarajan A Thandavarayan ◽  
Darukeshwara Joladarashi ◽  
Sahana Suresh Babu ◽  
Shashirekha Krishnamurthy ◽  
...  
Keyword(s):  
Heart Failure ◽  
High Glucose ◽  
Cardiac Tissue ◽  
Critical Role ◽  
Left Ventricular ◽  
Diabetic Patients ◽  
Therapeutic Implications ◽  
Caspase 1 ◽  
Ventricular Cardiomyocytes ◽  
Nlrp3 Expression

Diabetic cardiomyopathy is a common complication in patients with diabetes and is associated with underlying chronic inflammation and cardiac cell death, subsequently leading to left ventricular dysfunction and heart failure. ELAV-like protein 1 (ELAVL1, mRNA stabilizing protein) and NLRP3 activation (inflammasome complex protein)-mediated IL-1beta synthesis play a critical role in the progression of heart failure. However, ELAVL1 regulation of pyroptosis (caspase-1-mediated programmed apoptosis) and associated IL-1beta release in cardiomyocytes, especially under diabetic condition, remains elusive. Human diabetic, non-diabetic heart tissues, human ventricular cardiomyocytes and rat cardiomyoblasts exposed to high glucose (HG) were used for our studies. Our data demonstrates that human ventricular cardiomyocytes exposed to high glucose condition showed significant increase in ELAVL1 and NLRP3 expression with a concomitant increase in caspase-1 and IL-1 beta expression. Furthermore, human cardiac tissue from diabetic patients showed increased ELAVL1, caspase-1 and NLRP3 expression as compared to non-diabetic hearts. Intriguingly, ELAVL1 knockdown abrogates TNF-α induced canonical pyroptosis via NLRP3, caspase-1 and IL-1beta suppression. Interestingly, miRNA-9 expression significantly reduces in high glucose treated cardiomyocytes and in human diabetic hearts. Bioinformatics analysis and target validation assays showed that miR-9 directly targets ELAVL1. Inhibition of miR-9 up regulates ELAVL1 expression and activates caspase-1. Alternatively, miR-9 mimics attenuate hyperglycemia-induced ELAVL1 and inhibit cardiomyocyte pyroptosis. To our knowledge, this is the first report to demonstrate the role of miR-9/ELAVL1 in hyperglycemia-induced cardiac pyroptosis. Taken together our study highlights the potential therapeutic implications in preventing cardiomyocyte cell loss in human diabetic failing heart.

scholarly journals Neutrophil-Initiated Myocardial Inflammation and Its Modulation by B-Type Natriuretic Peptide: A Potential Therapeutic Target

2018 ◽  
Vol 20 (1) ◽  
pp. 129 ◽  
Author(s):  
Saifei Liu ◽  
Yuliy Chirkov ◽  
John Horowitz
Keyword(s):  
Heart Failure ◽  
Nadph Oxidase ◽  
Natriuretic Peptide ◽  
Tissue Injury ◽  
Diastolic Heart Failure ◽  
Cardiac Injury ◽  
Myocardial Inflammation ◽  
Inflammatory Disorder ◽  
Therapeutic Implications ◽  
Vasomotor Dysfunction

Activation of neutrophils is a critically important component of the innate immune response to bacterial and chemical stimuli, and culminates in the “neutrophil burst”, which facilitates neutrophil phagocytosis via the release of superoxide anion radical (O2−) from NADPH oxidase. Excessive and/or prolonged neutrophil activation results in substantial tissue injury and increases in vascular permeability—resulting in sustained tissue infiltration with neutrophils and monocytes, and persistent vasomotor dysfunction. Cardiovascular examples of such changes include acute and chronic systolic and diastolic heart failure (“heart failure with preserved ejection fraction”), and the catecholamine-induced inflammatory disorder takotsubo syndrome. We have recently demonstrated that B-type natriuretic peptide (BNP), acting via inhibition of activation of neutrophil NADPH oxidase, is an important negative modulator of the “neutrophil burst”, though its effectiveness in limiting tissue injury is partially lost in acute heart failure. The potential therapeutic implications of these findings, regarding the development of new means of treating both acute and chronic cardiac injury states, are discussed.

Sympathetic Activation in Congestive Heart Failure: Evidence, Consequences and Therapeutic Implications

2009 ◽  
Vol 7 (2) ◽  
pp. 137-145 ◽  
Author(s):  
Guido Grassi ◽  
Gino Seravalle ◽  
Fosca Quarti-Trevano ◽  
Raffaella Dell'Oro
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Sympathetic Activation ◽  
Therapeutic Implications

Endothelial dysfunction in chronic heart failure: clinical and therapeutic implications

2002 ◽  
Vol 13 (4) ◽  
pp. 233-239 ◽  
Author(s):  
Stamatis Adamopoulos ◽  
John T Parissis ◽  
Dimitrios Th Kremastinos
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Endothelial Dysfunction ◽  
Therapeutic Implications
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