Endothelium‐dependent contraction: The non‐classical action of endothelial prostacyclin, its underlying mechanisms, and implications

Liu, Bin; Zhou, Yingbi

doi:10.1096/fj.202101077r

Cited by 10 publications

(11 citation statements)

References 134 publications

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“…Some studies have shown that G protein-coupled receptor activation of the cAMP pathway is involved in PGI2-induced vasoconstriction (43) (Figure 4). In addition, Rucker et al showed that PGI and thromboxane are involved in maintaining vascular autostasis (44,45). Reduced PGI levels and increased thromboxane levels were found in constricted pulmonary arteries of patients with PH-LHD.…”

Section: Pgi2 Pathwaymentioning

confidence: 99%

Pathogenesis of pulmonary hypertension caused by left heart disease

Xiao

Lai

et al. 2023

Front. Cardiovasc. Med.

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Pulmonary hypertension has high disability and mortality rates. Among them, pulmonary hypertension caused by left heart disease (PH-LHD) is the most common type. According to the 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension, PH-LHD is classified as group 2 pulmonary hypertension. PH-LHD belongs to postcapillary pulmonary hypertension, which is distinguished from other types of pulmonary hypertension because of its elevated pulmonary artery wedge pressure. PH-LHD includes PH due to systolic or diastolic left ventricular dysfunction, mitral or aortic valve disease and congenital left heart disease. The primary strategy in managing PH-LHD is optimizing treatment of the underlying cardiac disease. Recent clinical studies have found that mechanical unloading of left ventricle by an implantable non-pulsatile left ventricular assist device with continuous flow properties can reverse pulmonary hypertension in patients with heart failure. However, the specific therapies for PH in LHD have not yet been identified. Treatments that specifically target PH in LHD could slow its progression and potentially improve disease severity, leading to far better clinical outcomes. Therefore, exploring the current research on the pathogenesis of PH-LHD is important. This paper summarizes and classifies the research articles on the pathogenesis of PH-LHD to provide references for the mechanism research and clinical treatment of PH-LHD, particularly molecular targeted therapy.

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Section: Pgi2 Pathwaymentioning

confidence: 99%

Pathogenesis of pulmonary hypertension caused by left heart disease

Xiao

Lai

et al. 2023

Front. Cardiovasc. Med.

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“…PGE2/E-prostanoid 3 receptor (EP3) signaling can mediate acute inflammatory J o u r n a l P r e -p r o o f 6 responses in disease models via the EP3/Gi/Ca 2+ influx signaling pathway 32,33 . We [34][35][36][37] and others 38 have elucidated that prostaglandins besides PGE2 can also activate EP3.…”

Section: Introductionmentioning

confidence: 95%

E-prostanoid 3 receptor deficiency on myeloid cells protects against ischemic acute kidney injury via breaking the auto-amplification loop of necroinflammation

Leng

Zhao²,

Guo³

et al. 2023

Kidney International

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“…No off-target sites were found in E. tenella genome with up to three nucleotides mismatch between the crRNA and potential off-target sites. Meanwhile, if there are more than two nucleotides mismatch, FnCas12a can efficiently distinguish and reject the off-target sites (Liu et al, 2021). Thus, we assume a high specificity of gene manipulation at the desired target locus.…”

Section: Fncas12a-mediated Knock-outmentioning

confidence: 99%

FnCas12a/crRNA-Mediated Genome Editing in Eimeria tenella

et al. 2021

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Eimeria species are intracellular parasites residing inside the intestinal epithelial cell, which cause poultry coccidiosis and result in significant financial losses in the poultry industry. Genome editing of Eimeria is of immense importance for the development of vaccines and drugs. CRISPR/Cas9 has been utilized for manipulating the genome of Eimeria tenella (E. tenella). Ectopic expression of Cas9, i.e., via plasmids, would introduce transgene, which substantially limits its application, especially for vaccine development. In this study, we initially optimized the condition of the transfection protocol. We demonstrated that with the optimized condition, the transfection of FnCas12a (also known as “FnCpf1”) protein and crRNA targeting EtHistone H4 triggered DNA double-strand breaks in vivo. We then used this strategy to knock-in a coding cassette for an enhanced yellow fluorescent protein (EYFP) and dihydrofolate reductase–thymidylate synthase gene (DHFR) as a selection marker to tag endogenous EtActin. The engineered E. tenella parasite possesses EYFP expression in its entire life cycle. Our results demonstrated that FnCas12a could trigger genome editing in E. tenella, which augments the applicability of the dissection of gene function and the development of anticoccidial drugs and vaccines for Eimeria species.

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Endothelium‐dependent contraction: The non‐classical action of endothelial prostacyclin, its underlying mechanisms, and implications

Abstract: This is an open access article under the terms of the Creat ive Commo ns Attri butio n-NonCo mmercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

Cited by 10 publications

References 134 publications

Pathogenesis of pulmonary hypertension caused by left heart disease

Pathogenesis of pulmonary hypertension caused by left heart disease

E-prostanoid 3 receptor deficiency on myeloid cells protects against ischemic acute kidney injury via breaking the auto-amplification loop of necroinflammation

FnCas12a/crRNA-Mediated Genome Editing in Eimeria tenella

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