Tanshinone IIA harmonizes the crosstalk of autophagy and polarization in macrophages via miR-375/KLF4 pathway to attenuate atherosclerosis

Chen, Wenna; Li, Ximing; Guo, Shengnan; Song, Nan; Wang, Junyan; Lu, Jia; Zhu, Aizhi

doi:10.1016/j.intimp.2019.02.054

Cited by 73 publications

(49 citation statements)

References 45 publications

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“…Studies have shown that some drugs can improve disease progression by promoting the phenotypic transformation of macrophages. For example, Tanshinone IIA can harmonizes the crosstalk of autophagy and macrophage polarization via the miR-375/ KLF4 pathway to attenuate atherosclerosis [31]. For SBP, the study found that cinnamic aldehyde inhibited the migration and M1 polarization of Raw264.7 macrophages induced by LPS [32].…”

Section: Discussionmentioning

confidence: 99%

Mechanism of angiogenesis promotion with Shexiang Baoxin Pills by regulating function and signaling pathway of endothelial cells through macrophages

et al. 2020

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Section: Discussionmentioning

confidence: 99%

Mechanism of angiogenesis promotion with Shexiang Baoxin Pills by regulating function and signaling pathway of endothelial cells through macrophages

et al. 2020

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“…Threose nucleic acid (TNA) is refractory to nuclease digestion and capable of undergoing Darwinian evolution to produce aptamers with affinity to specific targets. And, it could activate KLF4 and enhance autophagy as well as M2 polarization of macrophages by inhibiting miR‐375 to attenuate AS . miR‐21 restored impaired autophagic flux and lysosomal dysfunction, thereby attenuating ox‐LDL‐induced human aortic endothelial cells (HAECs) injuries in AS (Table ) …”

Section: Introductionmentioning

confidence: 99%

MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

et al. 2019

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Autophagy is a highly conserved catabolic process and fundamental biological process in eukaryotic cells. It recycles intracellular components to provide nutrients during starvation and maintains quality control of organelles and proteins. In addition, autophagy is a well‐organized homeostatic cellular process that is responsible for the removal of damaged organelles and intracellular pathogens. Moreover, it also modulates the innate and adaptive immune systems. Micro ribonucleic acids (microRNAs) are a mature class of post‐transcriptional modulators that are widely expressed in tissues and organs. And, it can suppress gene expression by targeting messenger RNAs for translational repression or, at a lesser extent, degradation. Research indicates that microRNAs regulate autophagy through different pathways, playing an essential role in the treatment of various diseases. It is an important regulator of fundamental cellular processes such as proliferation, autophagy, and cell apoptosis. In this review article, we first review the current knowledge of autophagy and the function of microRNAs. Then, we summarize the mechanism of autophagy and the signaling pathways related to autophagy by citing at least the main proteins involved in the different phases of the process. Second, we introduce other members of RNA and report some examples in various pathologies. Finally, we review the current literature regarding microRNA‐based therapies for cancer, atherosclerosis, cardiac disease, tuberculosis, and viral diseases. MicroRNAs can cause autophagy upregulation or downregulation by targeting genes or affecting autophagy‐related signaling pathways. Therefore, the microRNAs have a huge potential in autophagy regulation, and it is the function as diagnostic and prognostic markers.

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“…Besides, autophagy was reported to modulate the polarization conversion of macrophage phenotype [43]. The disorder of autophagy process had been indicated to be associated with the impairment of lipid clearance and pro-in ammatory phenotype formation of macrophages [43]. Based on this, we hypothesized that RVS mediated the activation of autophagy to encumber lipid accumulation and facilitate M2 phenotypic polarization of macrophages.…”

Section: Discussionmentioning

confidence: 93%

“…There was evidence demonstrating that autophagy activities were capable of weakening the extent of atheroma plaques via promoting cholesterol e ux of macrophages and then prohibiting foam cell formation [15,41,42]. Besides, autophagy was reported to modulate the polarization conversion of macrophage phenotype [43]. The disorder of autophagy process had been indicated to be associated with the impairment of lipid clearance and pro-in ammatory phenotype formation of macrophages [43].…”

Section: Discussionmentioning

confidence: 99%

Rosuvastatin Inhibits Atherosclerosis Development by Improving Lipid Accumulation and Polarization Conversion of Macrophages via Regulating Autophagy

Zhang¹,

Qin²,

Wan³

et al. 2020

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Background Atherosclerosis is a chronic vascular disease posing a great threat to public health. We investigated whether rosuvastatin (RVS) enhanced autophagic activities to inhibit lipid accumulation and polarization conversion of macrophages and then attenuate atherosclerotic lesions. Methods All male Apolipoprotein E-deficient (ApoE-/-) mice were fed high-fat diet supplemented with RVS (10mg/kg/day) or the same volume of normal saline gavage for 20 weeks. The burden of plaques in mice were determined by histopathological staining. Biochemical kits were used to examine the levels of lipid profiles and inflammatory cytokines. The potential mechanisms by which RVS mediated atherosclerosis were explored by western blot, real-time PCR assay, and immunofluorescence staining in mice and RAW264.7 macrophages.Results Our data showed that RVS treatment reduced plaque areas in the aorta inner surface and the aortic sinus of ApoE-/- mice with high-fat diet. RVS markedly improved lipid profiles and reduced contents of inflammatory cytokines in the circulation. Then, results of Western blot showed that RVS increased the ratio LC3II/I and level of Beclin 1 and decreased the expression of p62 in aortic tissues, which might be attributed to suppression of PI3K/Akt/mTOR pathway, hinting that autophagy cascades were activated by RVS. Moreover, RVS raised the contents of ABCA1, ABCG1, Arg-1, CD206 and reduced iNOS expression of arterial wall, indicating that RVS promoted cholesterol efflux and M2 macrophage polarization. Similarly, we observed that RVS decreased lipids contents and inflammatory factors expressions in RAW264.7 cells stimulated by ox-LDL, accompanied by levels elevation of ABCA1, ABCG1, Arg-1, CD206 and content reduction of iNOS. These anti-atherosclerotic effects of RVS were abolished by 3-methyladenine intervention. Moreover, RVS could reverse the impaired autophagy flux in macrophages insulted by chloroquine. We further found that PI3K inhibitor LY294002 enhanced and agonist 740 Y-P weakened the autophagy-promoting roles of RVS, respectively. Conclusions Our study indicated that RVS exhibits atheroprotective effects involving regulation lipid accumulation and polarization conversion by improving autophagy initiation and development via suppressing PI3K/Akt/mTOR axis and enhancing autophagic flux in macrophages.

show abstract

Tanshinone IIA harmonizes the crosstalk of autophagy and polarization in macrophages via miR-375/KLF4 pathway to attenuate atherosclerosis

Cited by 73 publications

References 45 publications

Mechanism of angiogenesis promotion with Shexiang Baoxin Pills by regulating function and signaling pathway of endothelial cells through macrophages

Mechanism of angiogenesis promotion with Shexiang Baoxin Pills by regulating function and signaling pathway of endothelial cells through macrophages

MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

Rosuvastatin Inhibits Atherosclerosis Development by Improving Lipid Accumulation and Polarization Conversion of Macrophages via Regulating Autophagy

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