CKLF1 aggravates neointimal hyperplasia by inhibiting apoptosis of vascular smooth muscle cells through PI3K/AKT/NF-κB signaling

Duan, Yanyu; Zhang, Yongbao; Qu, Chengjia; Yu, Weidong; Tana,; Shen, Chenyang

doi:10.1016/j.biopha.2019.108986

Cited by 8 publications

(11 citation statements)

References 44 publications

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“…It has been found that increased expression of CKLF1 on vascular smooth muscle cells would promote cell migration and proliferation, and further induce the appearance of atherosclerosis in mice. 23,30 The similar outcomes were also found in human samples. 48 Chen's laboratory conducted serial in-depth researches on the role of CKLF1 in cerebral ischemia/reperfusion injury.…”

Section: Relationships Between Cklf1 and Other Diseasessupporting

confidence: 77%

“…15 And through mediating vascular smooth muscle cells (VSMCs) migration, CKLF1 showed a boosting effect in intimal hyperplasia. 30 Considering that the relationships between CKLF1 and many human diseases have been reviewed before, we will take some different types of tumors as main examples here, to show the important but also complicated roles of CKLF1 in tumors and tumor development.…”

Section: Biological Functions Of Cklf1mentioning

confidence: 99%

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Chemokine-like factor 1: A promising therapeutic target in human diseases

Cai

Deng

Ming

et al. 2020

Exp Biol Med (Maywood)

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Chemokines are a family of small molecular-weight proteins, being well-known with their important roles in the process of allergic response, immune regulation, cell proliferation, and differentiation. Almost two decades ago, a novel member of this family, chemokine-like factor 1 (CKLF1) was identified. In recent years, it draws much attention of researchers because of its key roles in many types of tissues and its potential implications in a large number of diseases. Up to now, CKLF1 has been shown to have two main functions: broad-spectrum chemotactic activity, and proliferation- and differentiation-promoting abilities. In this review, we would introduce the basic structural features of CKLF1 and its biological functions, and then elaborate the relationships between CKLF1 and human diseases. The cell signaling pathways CKLF1 may be involved in would be discussed and summarized in details. Furthermore, we present the trials of CKLF1-targeted treatments in animal disease models, hoping to provide a few important insights about CKLF1 to both medical researchers and pharmacy, and finally conclude that CKLF1 is a potent, and very promising, therapeutic target. Impact statement CKLF1, a recently identified chemokine, has been reported by a number of studies to play important roles in quite many diseases. However, the potential pathways that CKLF1 may be involved are not manifested well yet. In our review, we showed the basic molecular structure and major functions of this novel chemokine, and implication in human diseases, such as tumors. To attract more attention, we summarized its signaling pathways and clearly present them in a set of figures. With the overview of the experimental trial of CKLF1-targeting medicines in animal models, we hope to provide a few important insights about CKLF1 to both medical researchers and pharmacy.

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Section: Relationships Between Cklf1 and Other Diseasessupporting

confidence: 77%

Section: Biological Functions Of Cklf1mentioning

confidence: 99%

Chemokine-like factor 1: A promising therapeutic target in human diseases

Cai

Deng

Ming

et al. 2020

Exp Biol Med (Maywood)

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“…Moreover, the accumulation of vascular smooth muscle cells (VSMCs) promotes plaque formation and development by migrating, proliferating, and secreting extracellular matrix to interact with other cellular components leading to the formation of plaques and thickening of the vascular wall, and finally a narrowing of the blood vessels (34)(35)(36). Studies have shown that the activation of the PI3K-Akt signaling pathway aggravates atherosclerotic injury in atherosclerosis mice (37), and has an inhibitory effect on the apoptosis of VSMCs (38). In view of the promotion effect of PI3K-Akt pathway on atherosclerosis and the increased expression of BCL2L1 (product of PI3K-Akt pathway), PI3K-Akt signaling pathway may be a crucial pathway to inhibit the apoptosis of VSMCs as well as accelerate the accumulation of plaque atherosclerosis, suggesting that inhibiting PI3K-Akt signaling pathway may be one of the pathways for XFZYD to treat atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Systematic Pharmacology and GEO Database Mining Revealed the Mechanism of XFZYD Therapy for ASCVD

Liang¹,

Xiang²,

Zhang³

et al. 2020

Preprint

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Background: Xuefu Zhuyu decoration (XFZYD), as a traditional Chinese compound recipe, has been used to treat atherosclerosis cardiovascular disease (ASCVD) for thousands of years in China, but its effective compounds and underlying treatment molecular mechanism remains promiscuous, which severely limits its clinical application. Methods : The effective components and its targets of XFZYD were predicted and screened based on the TCMSP database. The candidate therapeutic targets of ASCVD were screened by Pharmacogenomics Knowledgebase (PharmGKB) and Comparative Toxicogenomics Database (CTD). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses for target proteins were performed using DAVID database. Subsequently, protein-protein interaction (PPI) analyses were conducted using the STRING database. Differentially expressed genes in GSE71226 were identified using GEO2R. Finally, molecular docking was performed by Schrodinger software. Results: A total of 108 effective compounds and 137 candidate therapeutic targets were screened. Analyzing the relationships among effective compounds, candidate therapeutic targets, and signaling pathways, the therapy mechanism of XFZYD for ASCVD were mainly reflected in the protection of vascular endothelium, anti-inflammatory, antioxidant stress, etc. Moreover, the expression profile in GSE71226 supported our findings, while molecular simulation docking results also demonstrated the reliability of the predicted results. Conclusions: This study demonstrates the therapeutic potential of XFZYD for the treatment of ASCVD based on systemic pharmacology, which could provide a guiding principle for its clinical application as well as valuable insights for further drug discovery. Key words: Systematic pharmacology; atherosclerosis; Xuefu Zhuyu decoration; ASCVD

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“…Neointima formation is a process in three dimensions. But it is typically measured in two dimensions without an accurate 3D reconstruction [19][20][21]. Traditional 2D analyses cannot fully evaluate the spatial distribution of neointimal hyperplasia.…”

Section: Discussionmentioning

confidence: 99%

Effect of Endothelial Progenitor Cells Transplantation on Neointimal Hyperplasia and Reendothelialization after Balloon Catheter Injury in Rat Carotid Arteries

WANG

Zhang

Hui

et al. 2020

Preprint

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Background: Reendothelialization is a natural pathway to inhibit neointimal hyperplasia and in-stent restenosis. Circulating endothelial progenitor cells (EPCs) derived from bone marrow might contribute to endothelial repair. However, the temporal and spatial distribution of injured vascular reendothelialization and neointimal hyperplasia in the presence of transplanted EPCs is not quite clear. Methods: We performed a carotid balloon injury model and treated by transplantation of bone marrow-derived EPCs. To evaluate the temporal and spatial distribution of neointimal hyperplasia and reendothelialization after injury, the carotid arteries were harvested at different time points after transplantation. Results: Transplanted EPCs labeled by PKH26 were clearly observed attaching on the injured luminal surface at day 1 post-injury. For the undamaged arteries, the transplanted EPCs never adhered to the luminal surface. From day 4 post-injury, the average value of PKH26 fluorescence decreased significantly. Although transplanted EPCs were decreased significantly at the site of injury on day 4 after transplantation, reendothelialization at the site of the injury and inhibition of neointimal hyperplasia were significantly promoted by transplanted EPCs. The degree of reendothelialization of EPC7d (group of EPCs transplantation after balloon injury and harvested at day 7 post-transplantation)/EPC14d was significantly better than that of the BI7d (group of medium injection after balloon injury and harvested at day 7 post-injection)/BI14d, and the statistical difference of neointimal hyperplasia began to appear between EPC14d and BI14d. The number of endothelial cells on the lumen surface of EPC14d increased than that of BI14d, and the number of infiltrated macrophages at the injury site decreased.Conclusions: Transplanted EPCs had chemotactic enrichment and attached to the injured arterial intima after transplantation. Although decreased significantly at the site of injury over time after transplantation, transplanted EPCs could still promote the reendothelialization at the site of the injury and inhibition of neointimal hyperplasia.

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CKLF1 aggravates neointimal hyperplasia by inhibiting apoptosis of vascular smooth muscle cells through PI3K/AKT/NF-κB signaling

Cited by 8 publications

References 44 publications

Chemokine-like factor 1: A promising therapeutic target in human diseases

Chemokine-like factor 1: A promising therapeutic target in human diseases

Systematic Pharmacology and GEO Database Mining Revealed the Mechanism of XFZYD Therapy for ASCVD

Effect of Endothelial Progenitor Cells Transplantation on Neointimal Hyperplasia and Reendothelialization after Balloon Catheter Injury in Rat Carotid Arteries

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