SFRP4 Reduces Atherosclerosis Plaque Formation in ApoE Deficient Mice

Guan, Hua; Liu, Ting; Liu, Miaomiao; Wang, Xue; Shi, Tao; Guo, Fengwei

doi:10.1155/2023/8302289

Cited by 2 publications

(2 citation statements)

References 44 publications

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“…On the other hand, Wnt1 overexpression abolished the anti-atherosclerotic effect of SFRP4 in Apoe knockout mice [68]. Overexpression of SFRP4 induced by injection of adenoviral SFRP4 vector in ApoE knockout mice was associated with lowered lipid deposition in the whole aorta and aortic roots of these mice [69] (Table 1).…”

Section: Potential Strategies To Target Wnt Pathwaymentioning

confidence: 99%

“…Blocking all Wnt ligands could potentially inhibit all downstream signaling; however, simultaneous targeting of all Wnt ligands would not be practically feasible. Targeting of Wnt5a has shown some promising results in preclinical models [66][67][68][69]. Wnt5a is a ligand of the non-canonical Wnt pathway and blocking Wnt5a theoretically blocks the entire non-canonical Wnt signaling arm.…”

Section: Wnt Signaling Components As Therapeutic Targetsmentioning

confidence: 99%

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Wnt Signaling in Atherosclerosis: Mechanisms to Therapeutic Implications

Afroz,

Goodwin

2024

Biomedicines

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Atherosclerosis is a vascular disease in which inflammation plays a pivotal role. Receptor-mediated signaling pathways regulate vascular inflammation and the pathophysiology of atherosclerosis. Emerging evidence has revealed the role of the Wnt pathway in atherosclerosis progression. The Wnt pathway influences almost all stages of atherosclerosis progression, including endothelial dysfunction, monocyte infiltration, smooth muscle cell proliferation and migration, and plaque formation. Targeting the Wnt pathway to treat atherosclerosis represents a promising therapeutic approach that remains understudied. Blocking Wnt signaling utilizing small molecule inhibitors, recombinant proteins, and/or neutralizing antibodies ameliorates atherosclerosis in preclinical models. The Wnt pathway can be potentially manipulated through targeting Wnt ligands, receptors, co-receptors, and downstream signaling molecules. However, there are challenges associated with developing a real world therapeutic compound that targets the Wnt pathway. This review focuses on the role of Wnt signaling in atherosclerosis development, and the rationale for targeting this pathway for the treatment of atherosclerosis.

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Section: Potential Strategies To Target Wnt Pathwaymentioning

confidence: 99%

Section: Wnt Signaling Components As Therapeutic Targetsmentioning

confidence: 99%

Wnt Signaling in Atherosclerosis: Mechanisms to Therapeutic Implications

Afroz,

Goodwin

2024

Biomedicines

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Combining Bulk and Single Cell RNA-Sequencing Data to Identify Hub Genes of Fibroblasts in Dilated Cardiomyopathy

Huang,

Zhao,

et al. 2024

JIR

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Background Dilated cardiomyopathy (DCM) is the second leading cause of heart failure, with intricate pathophysiological underpinnings. In order to shed fresh light on the mechanistic research of DCM, we combined bulk RNA-seq and single-cell RNA-seq (scRNA-seq) data to examine significant cells and genes implicated in the disease. Methods This analysis employed publicly accessible bulk RNA-seq and scRNA-seq DCM datasets. The scRNA-seq data underwent normalization, principal component, and t-distribution stochastic neighbor embedding analysis. Cell-to-cell communication networks and activity analysis were conducted using CellChat. Utilizing enrichment analysis, the marker genes’ role in the active cells was evaluated. After screening by limma software and weighted gene co-expression network analysis, the differentially expressed genes (DEGs) served as hub genes. Furthermore, these hub genes were subjected to immunological studies, transcription factor expression, and gene set enrichment. Lastly, the expression of the four hub genes and their connection to DCM were verified using the rat models. Results Fibroblasts and monocytes were chosen as hub cells from among the eight identified cell clusters; their marker genes intersected with DEGs to yield six hub genes. In addition, the six hub genes and the essential module genes intersected to yield four essential genes ( ASPN, SFRP4, LUM , and FRZB) that were connected to the Wnt signaling pathway and highly expressed in fibroblast. The four hub DEGs had an expression pattern in the DCM rat model experiment results that was in line with the findings of the bioinformatics study. Additionally, there was a strong correlation between decreased cardiac function and the up-regulation of ASPN, SFRP4, LUM , and FRZB . Conclusion Ultimately, bulk RNA-seq and scRNA-seq data identified fibroblasts and monocytes as the main cell types implicated in DCM. The highly expressed genes ASPN, FRZB , LUM , and SFRP4 in fibroblasts may aid in the mechanistic investigation of DCM.

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SFRP4 Reduces Atherosclerosis Plaque Formation in ApoE Deficient Mice

Cited by 2 publications

References 44 publications

Wnt Signaling in Atherosclerosis: Mechanisms to Therapeutic Implications

Wnt Signaling in Atherosclerosis: Mechanisms to Therapeutic Implications

Combining Bulk and Single Cell RNA-Sequencing Data to Identify Hub Genes of Fibroblasts in Dilated Cardiomyopathy

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