Anti-Inflammatory Effects of Endothelin Receptor Antagonists and their Importance for Treating Human Disease

Barton, Matthias; Nett, Philipp C.; Amann, Kerstin; Teixeira, Mauro Martins

doi:10.2174/978160805160111001010236

Cited by 6 publications

(2 citation statements)

References 213 publications

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“…Under these disease conditions, increases in ET-1 are critically involved in initiating and maintaining inflammation and injury, thereby promoting perturbations among the rest of salt and water balance. At the renal level, ET-1 stimulates the aggregation and accumulation of neutrophils, thus propagating glomerular inflammation, a process that can be inhibited by ETA receptor blockade ( 113 ).…”

Section: The Contribution Of the Immune System To Heart Failurementioning

confidence: 99%

Involvement of Cytokines in the Pathogenesis of Salt and Water Imbalance in Congestive Heart Failure

et al. 2017

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Congestive heart failure (CHF) has become a major medical problem in the western world with high morbidity and mortality rates. CHF adversely affects several systems, mainly the kidneys and the lungs. While the involvement of the renin–angiotensin–aldosterone system and the sympathetic nervous system in the progression of cardiovascular, pulmonary, and renal dysfunction in experimental and clinical CHF is well established, the importance of pro-inflammatory mediators in the pathogenesis of this clinical setting is still evolving. In this context, CHF is associated with overexpression of pro-inflammatory cytokines, such as tumor necrosis factor-α, interleukin (IL)-1, and IL-6, which are activated in response to environmental injury. This family of cytokines has been implicated in the deterioration of CHF, where it plays an important role in initiating and integrating homeostatic responses both at the myocardium and circulatory levels. We and others showed that angiotensin II decreased the ability of the lungs to clear edema and enhanced the fibrosis process via phosphorylation of the mitogen-activated protein kinases p38 and p42/44, which are generally involved in cellular responses to pro-inflammatory cytokines. Literature data also indicate the involvement of these effectors in modulating ion channel activity. It has been reported that in heart failure due to mitral stenosis; there were varying degrees of vascular and other associated parenchymal changes such as edema and fibrosis. In this review, we will discuss the effects of cytokines and other inflammatory mediators on the kidneys and the lungs in heart failure; especially their role in renal and alveolar ion channels activity and fluid balance.

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Section: The Contribution Of the Immune System To Heart Failurementioning

confidence: 99%

Involvement of Cytokines in the Pathogenesis of Salt and Water Imbalance in Congestive Heart Failure

et al. 2017

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“…133 In chronic kidney disease, ET-1 has been shown to play an essential role in propagating glomerular inflammation, including accumulation of leukocytes, since these processes are inhibited by ET A receptor blockade. 134-136 In a rat model of mesangial proliferative glomerulonephritis, the infiltrating macrophages were the principal cells expressing ET-1 in glomeruli on day 1 after onset of disease. 81 In contrast to synthesis and secretion of ET-1 by infiltrated macrophages, ET-1 signaling and actions in immune cells which have infiltrated glomeruli have not been well studied.…”

Section: Glomerular Activities Of Endothelin In Health and Diseasementioning

confidence: 99%

Endothelin and the Glomerulus in Chronic Kidney Disease

Barton

Sorokin

2015

Seminars in Nephrology

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Summary Endothelin-1 (ET-1) is a 21-amino acid peptide with mitogenic and powerful vasoconstricting properties. Under healthy conditions, ET-1 is constitutively expressed in all cells of the glomerulus and participates in homeostasis of glomerular structure and filtration function. Under disease conditions, increases in ET-1 are critically involved in initiating and maintaining glomerular inflammation, glomerular basement membrane hypertrophy, and injury of podocytes (visceral epithelial cells), thereby promoting proteinuria and glomerulosclerosis. Here, we review the role of ET-1 in the function of glomerular endothelial cells, visceral (podocytes) and parietal epithelial cells, mesangial cells, the glomerular basement membrane, stromal cells, inflammatory cells, and mesenchymal stem cells. We also discuss molecular mechanisms by which ET-1 – predominantly through activation of the ETA receptor - contributes to injury to glomerular cells and review preclinical and clinical evidence supporting its pathogenic role in glomerular injury in chronic renal disease. Finally, the therapeutic rationale for endothelin antagonists as a new class of antiproteinuric drugs is discussed.

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Translational Vascular Medicine

Abraham¹,

Handler²,

Dashwood³

et al. 2012

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Anti-Inflammatory Effects of Endothelin Receptor Antagonists and their Importance for Treating Human Disease

Cited by 6 publications

References 213 publications

Involvement of Cytokines in the Pathogenesis of Salt and Water Imbalance in Congestive Heart Failure

Involvement of Cytokines in the Pathogenesis of Salt and Water Imbalance in Congestive Heart Failure

Endothelin and the Glomerulus in Chronic Kidney Disease

Translational Vascular Medicine

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