2019
DOI: 10.1016/j.ejphar.2019.172746
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Matrine pre-treatment suppresses AGEs- induced HCSMCs fibrotic responses by regulating Poldip2/mTOR pathway

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Cited by 15 publications
(7 citation statements)
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“…Advanced glycosylation end products (AGEs) are a group of substances existing in poorly controlled type 2 diabetes mellitus, which promote the fibrotic response of VSMCs and then aggravate AS through mTOR signaling pathway activation (de Vos et al, 2016). Matrine pretreatment reduced the expression of PI3K and the phosphorylation of mTOR in a concentration-dependent manner, as well as inhibited AGEs-induced fibrosis response in human coronary smooth muscle cells (HCSMCs) (Ma et al, 2019). The regulatory effect of matrine on mTOR provides a new idea for the treatment of type 2 diabetes-associated AS.…”
Section: Alkaloidsmentioning
confidence: 99%
“…Advanced glycosylation end products (AGEs) are a group of substances existing in poorly controlled type 2 diabetes mellitus, which promote the fibrotic response of VSMCs and then aggravate AS through mTOR signaling pathway activation (de Vos et al, 2016). Matrine pretreatment reduced the expression of PI3K and the phosphorylation of mTOR in a concentration-dependent manner, as well as inhibited AGEs-induced fibrosis response in human coronary smooth muscle cells (HCSMCs) (Ma et al, 2019). The regulatory effect of matrine on mTOR provides a new idea for the treatment of type 2 diabetes-associated AS.…”
Section: Alkaloidsmentioning
confidence: 99%
“…Matrine could down-regulate RyR2 expression, inhibit calcium overload caused by endoplasmic reticulum leakage to protect mitochondrial function, reduce age-induced heart injury and inhibit cardiomyocyte apoptosis (Wang et al, 2019a). Matrine could up-regulate poldip2 (polymerase δ Interacting protein2) expression, down-regulate Akt and mTOR phosphorylation, down-regulate phosphorylation level of downstream effector translation regulator P70S6K (70 kDa ribosomal S6 kinase), inhibit ECM protein expression, therefore, inhibit age-induced phenotypic transformation and fibrosis of HCMC (Ma et al, 2019).…”
Section: ) Anti-arrhythmia Activitymentioning
confidence: 99%
“…Zhang et al 45 demonstrated that matrine effectively improved lipid metabolism, inflammation, and vascular wall thickness in mice fed a high-fat diet, reduced the phosphorylation of nitric oxide synthase 3 (ENOS)-Thr497, and increased the phosphorylation of ENOS-S1177, thereby resulted in an increase in NO production, which is mediated by PI3K/AKT and protein kinase C Alpha (PKCα), revealing the molecular mechanism underlying the protective effect of matrine in high-fat diet-induced vascular disease. Ma et al 46 pre-treated human coronary smooth muscle cells (HCSMCs) with matrine and then exposed them to advanced glycation end products (AGEs). They found that matrine pre-treatment significantly reduced collagen content, increased smooth muscle myosin heavy chain 11 (MYH11) and DNA polymerase delta interacting protein 2 (Poldip2) expression, decreased the expressions of collagen I, β1-integrin, PI3K and nuclear p-p70S6k, and reduced the phosphorylation of AKT and mTOR in HCSMCs exposed to AGEs.…”
Section: Matrine Exerts Pharmacological Effects Through the Pi3k/akt/...mentioning
confidence: 99%