Salvianolic acid B ameliorates atherosclerosis via inhibiting YAP/TAZ/JNK signaling pathway in endothelial cells and pericytes

Yang, Ying; Pei, Ke; Zhang, Qian; Wang, Danyang; Feng, Huichao; Du, Ziwei; Zhang, Chunxiao; Gao, Zichen; Yang, Wenqing; Wu, Jibiao; Li, Yunlun

doi:10.1016/j.bbalip.2020.158779

Cited by 37 publications

(29 citation statements)

References 51 publications

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“…Further mechanistic studies showed that Sal-B inhibits of ox-LDL production possesses and anti-inflammatory functions by regulating the YAP/TAZ/JNK pathway. These results suggest that Sal-B inhibited YAP/TAZ activation and the subsequent JNK cascade to protect endothelial cells from inflammation in vitro and slow atherosclerosis development in vivo (105).…”

Section: Salvianolic Acid Bmentioning

confidence: 73%

Yes-Associated Protein in Atherosclerosis and Related Complications: A Potential Therapeutic Target That Requires Further Exploration

Sun

et al. 2021

Front. Cardiovasc. Med.

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Atherosclerosis and its complications diseases remain leading causes of cardiovascular morbidity and mortality, bringing a massive burden on public health worldwide. Atherosclerosis is recognized as chronic inflammation, and involves several highly correlated processes, including lipid metabolism dysfunction, endothelial cell dysfunction, inflammation, oxidative stress, vascular smooth muscle cell activation, platelet activation, thrombosis, altered matrix metabolism, and vascular remodeling. Within the past few decades, accumulating evidence has shown that the Yes-associated protein (YAP), the major effector of the Hippo pathway, can play a crucial role in pathogenesis and development of atherosclerosis. Activation of YAP-related pathways, which are induced by alerting flow pattern and matrix stiffness among others, can regulate processes including vascular endothelial cell dysfunction, monocyte infiltration, and smooth muscle cell migration, which contribute to atherosclerotic lesion formation. Further, YAP potentially modulates atherosclerotic complications such as vascular calcification and intraplaque hemorrhage, which require further investigation. Here, we summarized the relevant literature to outline current findings detailing the relationship between of YAP and atherosclerosis and highlight areas for future research.

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Section: Salvianolic Acid Bmentioning

confidence: 73%

Yes-Associated Protein in Atherosclerosis and Related Complications: A Potential Therapeutic Target That Requires Further Exploration

Sun

et al. 2021

Front. Cardiovasc. Med.

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“…Accumulation of foam cells and apoptosis leads to increased lipid core volume and thinning of the fibrous caps, resulting in rupture of vulnerable plaques. Studies showed that berberine maintained lipid homeostasis and reduced foam cells formation via LXRα/ABCA1 and Nrf/HO-1, limiting macrophage ox-LDL uptake and cholesterol efflux and inhibiting macrophages superoxide anion production ( Lee et al, 2010 ; Yang et al, 2020c ). Berberine also decreased endothelin-1 (ET-1) induced Lox-1 expression in monocyte-derived macrophages, acting as an antioxidant and reducing foam cell formation ( Chi et al, 2014 ; Caliceti et al, 2017 ).…”

Section: Tcm For Treatment Of Atherosclerosis Targeting Oxidative Stressmentioning

confidence: 99%

Chinese Herbal Medicines and Active Metabolites: Potential Antioxidant Treatments for Atherosclerosis

et al. 2021

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Atherosclerosis is a complex chronic disease that occurs in the arterial wall. Oxidative stress plays a crucial role in the occurrence and progression of atherosclerotic plaques. The dominance of oxidative stress over antioxidative capacity generates excess reactive oxygen species, leading to dysfunctions of the endothelium and accelerating atherosclerotic plaque progression. Studies showed that Chinese herbal medicines and traditional Chinese medicine (TCM) might regulate oxidative stress; they have already been used to treat diseases related to atherosclerosis, including stroke and myocardial infarction. This review will summarize the mechanisms of oxidative stress in atherosclerosis and discuss studies of Chinese herbal medicines and TCM preparations treating atherosclerosis, aiming to increase understanding of TCM and stimulate research for new drugs to treat diseases associated with oxidative stress.

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“…12 As a novel transcription factor, YAP can effectively enhance the expression of proinflammatory cytokines, accompanied by an increase in the expression level of tumor necrosis factor-α (TNF-α). 13,14 Inhibiting the expression of YAP or knocking out YAP can effectively down-regulate the expression of proinflammatory factors, 15 which indicated that YAP exerted an effective proinflammatory response. However, whether the pro-inflammatory response of YAP also inhibits the expression of anti-inflammatory factors such as IL-33 and IL-10 has not been reported.…”

Section: Introductionmentioning

confidence: 99%

Autophagy inhibition facilitates wound closure partially dependent on the YAP/IL‐33 signaling in a mouse model of skin wound healing

et al. 2021

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Autophagy is a self-phagocytic and highly evolutionarily conserved intracellular lysosomal catabolic system, which plays a vital role in a variety of trauma models, including skin wound healing (SWH). However, the roles and potential mechanisms of autophagy in SWH are still controversial. We firstly investigated the role of autophagy in SWH-induced wound closure rate, inflammatory response, and histopathology, utilizing an inhibitor of autophagy 3-methyladenine (3-MA) and

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Salvianolic acid B ameliorates atherosclerosis via inhibiting YAP/TAZ/JNK signaling pathway in endothelial cells and pericytes

Cited by 37 publications

References 51 publications

Yes-Associated Protein in Atherosclerosis and Related Complications: A Potential Therapeutic Target That Requires Further Exploration

Yes-Associated Protein in Atherosclerosis and Related Complications: A Potential Therapeutic Target That Requires Further Exploration

Chinese Herbal Medicines and Active Metabolites: Potential Antioxidant Treatments for Atherosclerosis

Autophagy inhibition facilitates wound closure partially dependent on the YAP/IL‐33 signaling in a mouse model of skin wound healing

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