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The Patient with Non-Group 2 Pulmonary Hypertension
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Sophia Anastasia Mouratoglou, George Giannakoulas
Selexipag is a selective prostacyclin IP receptor agonist available for oral administration at a starting dose of 200 μg twice daily, gradually up-titrated to the target dose of 1600 μg twice daily. The most common side effects are similar to those seen by other prostanoids. Selexipag reduced the composite of death, hospitalization for PAH worsening, disease progression, and listing for transplantation in a large, event-driven, randomized, trial, in which 80% of patients were on background oral PAH advanced treatment.76,77
The Role of Plant-Based Natural Compounds in Inflammation
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Marcela Dvorakova, Premysl Landa, Lenka Langhansova
Prostanoids are lipid mediators involved in a broad spectrum of physiological and pathological processes. They play a complex role in the normal function of kidneys, lungs, brain, ovaries, uterus, bones or the cardiovascular system. However, their synthesis is increased in inflamed tissue. Prostaglandins E2 (PGE2) and I2 (PGI2) are the main pro-inflammatory prostanoids enhancing edema formation and leukocyte infiltration. Moreover, they alter the threshold for pain perception. The application of COX inhibitors called non-steroidal anti-inflammatory drugs (NSAIDs) decreases prostanoid production. NSAIDs are used to relieve pain, fever and inflammation (Dubois et al., 1998; Smith et al., 2000; Smyth et al., 2009). Currently, NSAIDs belong to the most widely used pharmaceuticals consumed in tens of thousands of tons each year, especially as some of them are available over the counter (Warner and Mitchell, 2004).
Macronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Prostanoid includes prostaglandins (PGs) (PGD, PGE and PGF), thromboxane (TXA), and prostacyclin (PGI). These lipids are synthesized from the polyunsaturated fatty acids (PUFAs) dihomo-gamma-linolenic acid (DGLA, precursor of series 1 prostanoids), arachidonic acid (AA, precursor of series 2 prostanoids), and eicosapentaenoic acid (EPA, precursor of series 3 prostanoids). Among these precursors, AA is the most imperative and dominant in humans (102). Prostaglandins, thromboxane, and prostacyclin are universal lipids in animal tissues and organize several pathological and physiological processes. Prostaglandins (PGs) were discovered in 1935 as a blood-pressure-lowering matter from the prostate gland secretion (102). In 1976, prostacyclin was discovered as a powerful repressor of function of platelets, and as a robust vasodilator.
Plasma Cyclooxygenase-2 as a Potential Biomarker for Early Diagnosis of Kawasaki Disease
Published in Fetal and Pediatric Pathology, 2023
Cyclooxygenase-2 (COX-2) is an inducible isoenzyme of cyclooxygenase that converts arachidonic acid to prostaglandin endoperoxide H2, which is subsequently converted to different prostanoids including prostaglandins (PGD2, PGE2, PGF2α), prostacyclin (PGI2), or thromboxane A2 (TXA2) by tissue-specific enzymes. COX-2 is poorly expressed in most tissues under normal conditions but is highly induced by proinflammatory cytokines, growth factors, and hormones. COX-2 plays vital roles in the cardiovascular system through the multiple effects of prostanoids. There is growing evidence that prostanoids participate in the physiological and pathological processes of coronary arteries by regulating vascular tension, vascular remodeling, and angiogenesis [4]. Our previous research demonstrated the correlation between COX-2 gene polymorphisms and genetic susceptibility to KD [5]. However, changes of plasma COX-2 level during the course of KD remain unclear. The aim of this study was to detect the concentration of plasma COX-2 in patients with KD at a different stages of the disease, and determine whether COX-2 can be used as an effective biomarker to predict the CAL formation or therapeutic response to IVIG in KD children.
Epoprostenol for the treatment of pulmonary arterial hypertension
Published in Expert Review of Clinical Pharmacology, 2021
María José Cristo Ropero, Alejandro Cruz-Utrilla, María Pilar Escribano-Subias
Prostanoids can be divided into prostaglandins (PGD2, PGE2, PGI2 or prostacyclin, and PGF2) and thromboxane. They act on G-protein-coupled prostanoid IP receptors. Within the pulmonary vasculature, these receptors could be categorized as relaxant (IP, DP1, EP2, EP4) and contractile receptors (EP1, EP3, FP, and TP). Prostacyclin synthase produces prostacyclin within vascular endothelial cells. Epoprostenol acts as a synthetic analog of prostaglandin I2 in endothelial cells with a vasodilatory effect. The receptor’s activation in other cells produces anti-inflammatory, antiaggregating, and antiproliferative effects (Figure 1). Also, smooth muscle cell proliferation is slowed via transformation of ATP to AMP and an increase in protein kinase A activity. Two main metabolites of have been identified as follows: 6-keto-prostacyclin F1α, the more suitable marker of plasma concentrations of the drug and formed by hydration; and 6,15-diketo-13,14-dihydro-prostacyclin F1α, produced by enzymatic degradation. This drug has a short elimination half-life (3–6 minutes) in the human blood stream [42].
Selexipag for the treatment of pulmonary arterial hypertension
Published in Expert Review of Respiratory Medicine, 2021
Léon Genecand, Julie Wacker, Maurice Beghetti, Frédéric Lador
Cyclooxygenase metabolizes arachidonic acid (AA) into PGI2,Prostaglandin D2, prostaglandin E2, prostaglandin G2a, and thromboxane, regrouped under the term ‘prostanoids’ [7]. Prostanoids act via their receptors including prostaglandin D receptor, prostaglandin E receptor (1–4), prostaglandin F receptor, and PGI2 receptor (IP receptor). Vascular endothelial cells are the main producers of PGI2, which act mainly via the IP receptor leading to vasodilatation, antiplatelet and antiproliferative actions [7]. Reductions of PGI2 urinary metabolites and of PGI2 synthase expression in the pulmonary arteries have been shown in PAH patients [8]. Nonspecific binding of PGI2 to prostaglandin receptors in the gastric mucosa has been described and could explain some side effects [9].