Lupeol protects against cardiac hypertrophy via TLR4-PI3K-Akt-NF-κB pathways

Li, Dan; Guo, Yingying; Cen, Xian-feng; Qiu, Hong-liang; Chen, Si; Zeng, Xiaofeng; Zeng, Qian; Xu, Man; Tang, Qi‐Zhu

doi:10.1038/s41401-021-00820-3

Cited by 41 publications

(12 citation statements)

References 49 publications

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“…Next, 740 Y-P, a PI3K agonist, 23 was applied to explore the association between PI3K/AKT signaling and SORT1 in the regulation of malignant behaviors of HCC cells. SNU449 and HEP3B cells were divided into three groups: sh-NC, sh-SORT1#1, and sh-SORT1#1 + 740 Y-P.…”

Section: Resultsmentioning

confidence: 99%

Sortilin 1 regulates hepatocellular carcinoma progression by activating the PI3K/AKT signaling

Wang

Zhou

et al. 2022

Hum Exp Toxicol

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Background Sortilin 1 (SORT1) has been reported as an oncogene in several human tumors. Nonetheless, the biological functions of SORT1 in hepatocellular carcinoma (HCC) remain poorly understood. Methods Western blotting was employed for the determination of protein expression. Hepatocellular carcinoma cell viability, apoptosis, migration, and invasion were measured via CCK-8, flow cytometry, wound healing, and Transwell assays. Results Sortilin 1 was upregulated in HCC and closely associated with unsatisfactory outcomes of HCC patients. Furthermore, in vitro and in vivo assays revealed that SORT1 knockdown significantly diminished HCC cell proliferation and metastasis but accelerated HCC cell apoptosis; moreover, SORT1 depletion also restrained the growth of xenografted HCC tumors. Mechanistically, SORT1 activated PI3K/AKT signaling in HCC cells, thereby promoting the malignant behaviors of HCC cells. Conclusion This study demonstrated that SORT1 might promote HCC progression by activating PI3K/AKT signaling, indicating that SORT1 might be a promising target and biomarker for HCC treatment and prognosis.

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Section: Resultsmentioning

confidence: 99%

Sortilin 1 regulates hepatocellular carcinoma progression by activating the PI3K/AKT signaling

Wang

Zhou

et al. 2022

Hum Exp Toxicol

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“…TLR proteins are pattern recognition receptors for multiple pathogens, including SARS-CoV-2 and MPXV [22] , [34] . In this study, the TLR2 agonist Pam2Cys and TLR4 agonist RS-09 were included in the S7M8 vaccine to trigger activation of TLR2 and TLR4 signaling [81] , [82] , [83] , [84] , [85] , [86] . Furthermore, our results suggested that the S7M8 vaccine could stably bind to TLR2 and TLR4, which laid the foundation for the S7M8 vaccine to recognize and activate TLR pathways effectively.…”

Section: Discussionmentioning

confidence: 99%

Developing a multiepitope vaccine for the prevention of SARS-CoV-2 and monkeypox virus co-infection: A reverse vaccinology analysis

Jiang

Liu

Xue

et al. 2023

International Immunopharmacology

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“… 4 , 39 Meanwhile, inflammatory cytokines serve as crucial biomarkers that can predict the incidence and prognosis of AF. 39 Pressure overload leads to an increase in a series of inflammatory cytokines in the heart, such as TNF-α, IL-1β, and IL-6, 40 , 41 which not only accelerate the progression of pathological cardiac remodelling but also promote the secretion of inflammatory cytokines by recruiting more inflammatory cells to the heart. 41 Overexpression of TNF-α causes abnormal Ca 2+ release and handling in the atrial myocardium and then increases vulnerability to AF.…”

Section: Discussionmentioning

confidence: 99%

“… 39 Pressure overload leads to an increase in a series of inflammatory cytokines in the heart, such as TNF-α, IL-1β, and IL-6, 40 , 41 which not only accelerate the progression of pathological cardiac remodelling but also promote the secretion of inflammatory cytokines by recruiting more inflammatory cells to the heart. 41 Overexpression of TNF-α causes abnormal Ca 2+ release and handling in the atrial myocardium and then increases vulnerability to AF. 42 , 43 Pressure overload did not lead to an increase in the induction rate of AF in IL-1β knockout mice, suggesting that IL-1β plays a vital role in pressure overload-induced AF.…”

Section: Discussionmentioning

confidence: 99%

Ubiquitin-specific protease 38 promotes inflammatory atrial fibrillation induced by pressure overload

Xiao,

Pan,

Kong

et al. 2023

Europace

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Aims Atrial structural and electrical remodelling is a major reason for the initiation and perpetuation of atrial fibrillation (AF). Ubiquitin-specific protease 38 (USP38) is a deubiquitinating enzyme, but its function in the heart remains unknown. The aim of this study was to investigate the effect of USP38 in pressure overload-induced AF. Methods and results Cardiac-specific knockout USP38 and cardiac-specific transgenic USP38 mice and their corresponding control mice were used in this study. After 4 weeks with or without aortic banding (AB) surgery, atrial echocardiography, atrial histology, electrophysiological study, and molecular analysis were assessed. Ubiquitin-specific protease 38 knockout mice showed a remarkable improvement in vulnerability to AF, atrial weight and diameter, atrial fibrosis, and calcium-handling protein expression after AB surgery. Conversely, USP38 overexpression further increased susceptibility to AF by exacerbating atrial structural and electrical remodelling. Mechanistically, USP38 interacted with and deubiquitinated nuclear factor-kappa B (NF-κB), and USP38 overexpression increased the level of p-NF-κB in vivo and in vitro, accompanied by the upregulation of NOD-like receptor protein 3 (NLRP3) and inflammatory cytokines, suggesting that USP38 contributes to adverse effects by driving NF-κB/NLRP3-mediated inflammatory responses. Conclusion Overall, our study indicates that USP38 promotes pressure overload-induced AF through targeting NF-κB/NLRP3-mediated inflammatory responses.

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Lupeol protects against cardiac hypertrophy via TLR4-PI3K-Akt-NF-κB pathways

Cited by 41 publications

References 49 publications

Sortilin 1 regulates hepatocellular carcinoma progression by activating the PI3K/AKT signaling

Sortilin 1 regulates hepatocellular carcinoma progression by activating the PI3K/AKT signaling

Developing a multiepitope vaccine for the prevention of SARS-CoV-2 and monkeypox virus co-infection: A reverse vaccinology analysis

Ubiquitin-specific protease 38 promotes inflammatory atrial fibrillation induced by pressure overload

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