Chaetocin attenuates atherosclerosis progression and inhibits vascular smooth muscle cell phenotype switching

Chen, Mingyun; Zhang, Zhihui; Ke, Jiang-Feng; Li, Tingting; Li, Meifang; Lu, Junxi; Li, Lianxi

doi:10.1007/s12265-022-10258-5

Cited by 4 publications

(3 citation statements)

References 41 publications

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“…44,45 Chaetocin, an inhibitor of H3K9 methyltransferase SUV39H, inhibits SUV39H and decreases the expression of matrix metalloproteinase 9 (MMP9). 46 Panobinostat decreases highsensitivity C-reactive protein (hsCRP), soluble CD40 ligand (sCD40L), MMP-9, IL-6 as well as total circulating monocytes, romidepsin decreases monocytic adhesion to arterial EC, sodium butyrate downregulates inflammatory mediators such as TNF-α, IL-6, and HMGB1, while GSK126 inhibits lipid formation in both THP-1 and RAW264.7derived macrophages. [47][48][49][50] The BET protein inhibitor apabetalone (RVX-208) has been found to counter proinflammatory aortic gene expression in a diet-induced obesity mouse model and in human endothelial cells.…”

Section: Histone Modification-based Atherosclerosis Pharmacotherapymentioning

confidence: 99%

Recent Updates on Epigenetic-Based Pharmacotherapy for Atherosclerosis

Ariyanto,

Wijaya,

Pradian

et al. 2024

DMSO

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Atherosclerosis is one of the most dominant pathological processes responsible in cardiovascular diseases (CVD) caused by cholesterol accumulation accompanied by inflammation in the arteries which will subsequently lead to further complications, including myocardial infarction and stroke. Although the incidence of atherosclerosis is decreasing in some countries, it is still considered the leading cause of death worldwide. Atherosclerosis is a vascular pathological process that is chronically inflammatory and is characterized by the invasion of inflammatory cells and cytokines. Many reports have unraveled the pivotal roles of epigenetics such as DNA methylation, post-translational histone modifications, and non-coding RNAs (ncRNAs) in atherogenesis, which regulate the expression of numerous genes related to various responsible pathways. Many studies have been conducted to develop new therapeutical approaches based on epigenetic changes for combating atherosclerosis. This review elaborates on recent updates on the development of new atherosclerosis drugs whose mechanism of action is associated with the modulation of DNA methylation, posttranslational histone modifications, and ncRNA-based gene regulation.

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Section: Histone Modification-based Atherosclerosis Pharmacotherapymentioning

confidence: 99%

Recent Updates on Epigenetic-Based Pharmacotherapy for Atherosclerosis

Ariyanto,

Wijaya,

Pradian

et al. 2024

DMSO

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“…AS is a chronic inflammatory disease characterized by the formation of plaques within the arterial intima ( 17 ). Compared to VSMCs in healthy vessels, those in AS exhibit reduced expression of contractile molecules such as SM22 and α-SMA, while the expression of secretory markers like OPN and MMPs is increased ( 78 ). Genetic tracing studies have shown that about 70% of VSMCs in AS plaques originate from the phenotypic transformation, proliferation, and migration of medial VSMCs, thereby contributing to plaque formation ( 79 ).…”

Section: Introductionmentioning

confidence: 99%

Elucidating VSMC phenotypic transition mechanisms to bridge insights into cardiovascular disease implications

Xin,

Zhang,

et al. 2024

Front. Cardiovasc. Med.

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Cardiovascular diseases (CVD) are the leading cause of death worldwide, despite advances in understanding cardiovascular health. Significant barriers still exist in effectively preventing and managing these diseases. Vascular smooth muscle cells (VSMCs) are crucial for maintaining vascular integrity and can switch between contractile and synthetic functions in response to stimuli such as hypoxia and inflammation. These transformations play a pivotal role in the progression of cardiovascular diseases, facilitating vascular modifications and disease advancement. This article synthesizes the current understanding of the mechanisms and signaling pathways regulating VSMC phenotypic transitions, highlighting their potential as therapeutic targets in cardiovascular disease interventions.

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“…Chaetocin is a small molecular compound isolated from the marine fungus genus Chaetomium. Previous studies have revealed that chaetocin has multiple pharmacological activities, such as antiviral, antiparasitic, anti-gout and cardiovascular protective effects [17][18][19][20]. We have reviewed recent studies showing that chaetocin exhibits potent inhibitory effects against a variety type of cancers [21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Chaetocin exhibits anticancer effects in esophageal squamous cell carcinoma via activation of hippo pathway

Liu

Jiang

Li³

et al. 2023

Aging

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Dysfunction of the Hippo pathway is common in esophageal squamous carcinoma (ESCC). Chaetocin, a small molecular compound isolated from the marine fungus, exhibits potent anticancer effects. However, the anticancer effects of chaetocin on ESCC and its potential relationship to Hippo pathway remain unclear. Here, we demonstrated that chaetocin dramatically inhibited the proliferation in ESCC cells by causing cycle arrest in the M phase and activating the caspase-dependent apoptosis signaling pathway in vitro , and we also found that chaetocin induced the accumulation cellular reactive oxygen species (ROS). The RNA-seq analysis indicated that the Hippo pathway is one of the most enriched pathways after chaetocin treatment. We further revealed that chaetocin triggered the activation of Hippo pathway in ESCC cells, which is characterized by elevated phosphorylation levels of almost all core proteins in Hippo pathway, such as MST1 (Thr183), MST2 (Thr180), MOB1 (Thr35), LAST1 (Thr1079 and Ser909) and YAP (Ser127), ultimately leading to decreased nuclear translocation of YAP. Moreover, the MST1/2 inhibitor XMU-MP-1 not only partially rescued the inhibitory effect chaetocin-induced proliferation, but also rescued the chaetocin-induced apoptosis in ESCC cells. Furthermore, in vivo results confirmed the antitumor effect of chaetocin and its relationship with Hippo pathway. Taken together, our study demonstrates that chaetocin exhibits anticancer effects in ESCC via activation of Hippo pathway. These results provide an important basis for further research of chaetocin as a potential candidate for ESCC treatment.

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Chaetocin attenuates atherosclerosis progression and inhibits vascular smooth muscle cell phenotype switching

Cited by 4 publications

References 41 publications

Recent Updates on Epigenetic-Based Pharmacotherapy for Atherosclerosis

Recent Updates on Epigenetic-Based Pharmacotherapy for Atherosclerosis

Elucidating VSMC phenotypic transition mechanisms to bridge insights into cardiovascular disease implications

Chaetocin exhibits anticancer effects in esophageal squamous cell carcinoma via activation of hippo pathway

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