2023
DOI: 10.3390/ijms24044193
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The Link between Prostanoids and Cardiovascular Diseases

Abstract: Cardiovascular diseases are the leading cause of global deaths, and many risk factors contribute to their pathogenesis. In this context, prostanoids, which derive from arachidonic acid, have attracted attention for their involvement in cardiovascular homeostasis and inflammatory processes. Prostanoids are the target of several drugs, but it has been shown that some of them increase the risk of thrombosis. Overall, many studies have shown that prostanoids are tightly associated with cardiovascular diseases and … Show more

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Cited by 24 publications
(19 citation statements)
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“…It functions in the relaxation and contraction of smooth muscle cells and platelet aggregation. Consistent with our findings, studies have demonstrated that the PTGD gene is downregulated in smokers and associated with smoking and plaque development [ 47 , 48 ]. A mouse model also highlighted the involvement of PTGDS in promoting thrombosis [ 47 ].…”
Section: Discussionsupporting
confidence: 93%
“…It functions in the relaxation and contraction of smooth muscle cells and platelet aggregation. Consistent with our findings, studies have demonstrated that the PTGD gene is downregulated in smokers and associated with smoking and plaque development [ 47 , 48 ]. A mouse model also highlighted the involvement of PTGDS in promoting thrombosis [ 47 ].…”
Section: Discussionsupporting
confidence: 93%
“…Prostaglandins constitute a group of ubiquitous, naturally occurring substances that exhibit a notably broad range of biological effects, particularly within the cardiovascular system. In this context, they play pivotal roles in the regulation of vascular constriction, cardiac restructuring, and inflammatory responses [ 45 , 46 ]. HPGD encodes 15-PGDH, an enzyme that regulates prostaglandin E2 (PGE2) metabolism and is crucial for inflammation control.…”
Section: Discussionmentioning
confidence: 99%
“…Of these GPCRs, we aimed to further characterize Ptgfr , as this GPCR (i) shows a significantly increased expression level in failing vs. normal rat and human hearts, as also shown by the single-nucleus transcriptomic data of human failing hearts from patients with dilated or hypertrophic cardiomyopathy [ 34 ] (available through the Broad Institute’s Single Cell Portal under project ID SCP1303), a finding that supports potential translatability into the clinical settings, (ii) has a high abundance in the cardiac tissue, and especially on cardiac ventricular fibroblast and cardiomyocytes (iii) can be targeted by a highly selective commercially available antagonist, AL-8810, and (iv) is novel to be described in the context of HF and cardiomyocyte hypertrophy. Previous publications also evidence that prostaglandin-F2α (PGF2α)- Ptgfr axis may play a pivotal role in cardiovascular diseases [ 35 , 36 ]. An early study by Rabinowitz and colleagues described that PGF2α is mainly produced by cardiac fibroblasts, which increases via myocardial ischemia [ 37 ].…”
Section: Discussionmentioning
confidence: 99%