Effect and mechanism of apelin on lipopolysaccharide induced acute pulmonary vascular endothelial barrier dysfunction

Huang, Tianpeng; Chen, Danyang; Ye, Wei; Chen, Wenwen; Zhang, Min; Hao, Jia-le; Xu, Licong; Bai, Xiaoqing; Mao, Sun‐Zhong

doi:10.1038/s41598-023-27889-6

Cited by 3 publications

(1 citation statement)

References 30 publications

(33 reference statements)

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“…Apelin treatment reverses these effects and decreases internalization of VE-cadherin, thus increasing barrier stability. Inhibition of FLI-1 reduces the benefit of apelin treatment [ 51 ]. As such, the apelin-APR signalling axis may be an important therapeutic target to increase junctional integrity and endothelial barrier stability during acute lung injury caused by infections.…”

Section: Host Modulation Strategiesmentioning

confidence: 99%

Modulation of the Host Response as a Therapeutic Strategy in Severe Lung Infections

Latreille

Lee

2023

Viruses

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Respiratory pathogens such as influenza and SARS-CoV-2 can cause severe lung infections leading to acute respiratory distress syndrome (ARDS). The pathophysiology of ARDS includes an excessive host immune response, lung epithelial and endothelial cell death and loss of the epithelial and endothelial barrier integrity, culminating in pulmonary oedema and respiratory failure. Traditional approaches for the treatment of respiratory infections include drugs that exert direct anti-pathogen effects (e.g., antivirals). However, such agents are typically ineffective or insufficient after the development of ARDS. Modulation of the host response has emerged as a promising alternative therapeutic approach to mitigate damage to the host for the treatment of respiratory infections; in principle, this strategy should also be less susceptible to the development of pathogen resistance. In this review, we discuss different host-targeting strategies against pathogen-induced ARDS. Developing therapeutics that enhance the host response is a pathogen-agnostic approach that will help prepare for the next pandemic.

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Section: Host Modulation Strategiesmentioning

confidence: 99%

Modulation of the Host Response as a Therapeutic Strategy in Severe Lung Infections

Latreille

Lee

2023

Viruses

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Apelin modulates inflammation and leukocyte recruitment in experimental autoimmune encephalomyelitis

Park,

Song,

Jeong

et al. 2024

Nat Commun

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Demyelination due to autoreactive T cells and inflammation in the central nervous system are principal features of multiple sclerosis (MS), a chronic and highly disabling human disease affecting brain and spinal cord. Here, we show that treatment with apelin, a secreted peptide ligand for the G protein-coupled receptor APJ/Aplnr, is protective in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Apelin reduces immune cell entry into the brain, delays the onset and reduces the severity of EAE. Apelin affects the trafficking of leukocytes through the lung by modulating the expression of cell adhesion molecules that mediate leukocyte recruitment. In addition, apelin induces the internalization and desensitization of its receptor in endothelial cells (ECs). Accordingly, protection against EAE major outcomes of apelin treatment are phenocopied by loss of APJ/Aplnr function, achieved by EC-specific gene inactivation in mice or knockdown experiments in cultured primary endothelial cells. Our findings highlight the importance of the lung-brain axis in neuroinflammation and indicate that apelin targets the transendothelial migration of immune cells into the lung during acute inflammation.

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FLI-1-driven regulation of endothelial cells in human diseases

Zhang,

Ge,

Cui

2024

J Transl Med

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Endothelial cells (ECs) are widely distributed in the human body and play crucial roles in the circulatory and immune systems. ECs dysfunction contributes to the progression of various chronic cardiovascular, renal, and metabolic diseases. As a key transcription factor in ECs, FLI-1 is involved in the differentiation, migration, proliferation, angiogenesis and blood coagulation of ECs. Imbalanced FLI-1 expression in ECs can lead to various diseases. Low FLI-1 expression leads to systemic sclerosis by promoting fibrosis and vascular lesions, to pulmonary arterial hypertension by promoting a local inflammatory state and vascular lesions, and to tumour metastasis by promoting the EndMT process. High FLI-1 expression leads to lupus nephritis by promoting a local inflammatory state. Therefore, FLI-1 in ECs may be a good target for the treatment of the abovementioned diseases. This comprehensive review provides the first overview of FLI-1-mediated regulation of ECs processes, with a focus on its influence on the abovementioned diseases and existing FLI-1-targeted drugs. A better understanding of the role of FLI-1 in ECs may facilitate the design of more effective targeted therapies for clinical applications, particularly for tumour treatment.

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Effect and mechanism of apelin on lipopolysaccharide induced acute pulmonary vascular endothelial barrier dysfunction

Cited by 3 publications

References 30 publications

Modulation of the Host Response as a Therapeutic Strategy in Severe Lung Infections

Modulation of the Host Response as a Therapeutic Strategy in Severe Lung Infections

Apelin modulates inflammation and leukocyte recruitment in experimental autoimmune encephalomyelitis

FLI-1-driven regulation of endothelial cells in human diseases

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