Autophagy enhanced by curcumin ameliorates inflammation in atherogenesis via the TFEB–P300–BRD4 axis

Li, Xuesong; Zhu, Ruigong; Jiang, Hong; Yin, Quanwen; Gu, Jiaming; Chen, Jiajing; Ji, Xiuqing; Wu, Xuan; Fu, Haiping; Wang, Hui; Tang, Xin; Gao, Yuanqing; Wang, Bingjian; Ji, Yong; Chen, Hongshan

doi:10.1016/j.apsb.2021.12.014

Cited by 46 publications

(27 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…TFEB nuclear translocation was detected by immunofluorescence 33 . The cell slides were fixed for 5 min in 100% methanol, treated for 30 min with 0.5% Triton X‐100, and blocked for 30 min with normal goat serum at room temperature.…”

Section: Methodsmentioning

confidence: 99%

“…TFEB nuclear translocation was detected by immunofluorescence. 33 The cell slides were fixed for 5 min in 100% methanol, treated for 30 min with 0.5% Triton X-100, and blocked for 30 min with normal goat serum at room temperature. The cells were then incubated overnight with primary antibody anti-TFEB (Abcam) at 4 C, rinsed with PBS, incubated with Alexa Fluor 594-labeled IgG H&L (red fluorescence, 2 μg/mL, ab150080, Abcam) in the dark for 30 min at room temperature, and subjected to DAPI (blue, ab104139, Abcam) staining to stain the nuclear DNA.…”

Section: Immunofluorescencementioning

confidence: 99%

See 1 more Smart Citation

Naringenin facilitates M2 macrophage polarization after myocardial ischemia–reperfusion by promoting nuclear translocation of transcription factor EB and inhibiting the NLRP3 inflammasome pathway

Liu

et al. 2023

Environmental Toxicology

View full text Add to dashboard Cite

Myocardial ischemia–reperfusion injury (MIRI) remains an unsolved puzzle in medical circles. Naringenin (NAR) is a flavonoid with cardioprotective potential. The purpose of this article was to discuss the protective mechanism of NAR in MIRI by regulating macrophage polarization. The MIRI mouse model was established and perfused with NAR before surgery. In the in vitro experiment, macrophages RAW264.7 were treated with lipopolysaccharide to induce M1 polarization after pretreatment with NAR. Rescue experiments were carried out to validate the functions of transcription factor EB (TFEB), the NLR pyrin domain containing 3 (NLRP3) inflammasome, and autophagy in macrophage polarization. NAR reduced histopathological injury and infarction of myocardial tissues in MIRI mice, inhibited M1 polarization and promoted M2 polarization of macrophages, diminished levels of pro‐inflammatory factors, and augmented levels of anti‐inflammatory factors. NAR facilitated TFEB nuclear translocation and inhibited the NLRP3 inflammasome pathway. Silencing TFEB or Nigericin partly nullified the effect of NAR on macrophage polarization. NAR increased autophagosome formation, autophagy flux, and autophagy level. Autophagy inhibitor 3‐methyladenine partly invalidated the inhibition of NAR on the NLRP3 inflammasome pathway. In animal experiments, NAR protected MIRI mice through the TFEB‐autophagy‐NLRP3 inflammasome pathway. Collectively, NAR inhibited NLRP3 inflammasome activation and facilitated M2 macrophage polarization by stimulating TFEB nuclear translocation, thus protecting against MIRI.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Immunofluorescencementioning

confidence: 99%

Naringenin facilitates M2 macrophage polarization after myocardial ischemia–reperfusion by promoting nuclear translocation of transcription factor EB and inhibiting the NLRP3 inflammasome pathway

Liu

et al. 2023

Environmental Toxicology

View full text Add to dashboard Cite

show abstract

“…Curcumin can function as an anti-inflammatory agent by blocking NF- κ B and STAT3-mediated inflammatory response signaling pathways, and preventing the development of inflammation-related chronic diseases 98 , 99 . Curcumin significantly improves atherosclerosis 100 . Curcumin and its metabolites extend the lifespans of nematodes, drosophila, and mice.…”

Section: Natural Products In the Treatment Of Inflammatory Diseases A...mentioning

confidence: 99%

New opportunities and challenges of natural products research: When target identification meets single-cell multiomics

Zhu

Ouyang

et al. 2022

Acta Pharmaceutica Sinica B

187

View full text Add to dashboard Cite

“…Similarly, curcumin plays an important role in attenuating atherosclerotic endothelial cell injury by regulating the autophagy-related PI3K/AMPK/mTOR/p70S6K signaling pathway (Zhao et al, 2021). Curcumin promotes autophagy and reduces inflammation by promoting nuclear translocation in TFEB, one of the downstream factors of mTORC1 (Li et al, 2022). However, whether curcumin can regulate TFEB through mTOR still needs more specific studies.…”

Section: Polyphenolsmentioning

confidence: 99%

Natural compounds from botanical drugs targeting mTOR signaling pathway as promising therapeutics for atherosclerosis: A review

Liu

et al. 2023

Front. Pharmacol.

View full text Add to dashboard Cite

Atherosclerosis (AS) is a chronic inflammatory disease that is a major cause of cardiovascular diseases (CVDs), including coronary artery disease, hypertension, myocardial infarction, and heart failure. Hence, the mechanisms of AS are still being explored. A growing compendium of evidence supports that the activity of the mechanistic/mammalian target of rapamycin (mTOR) is highly correlated with the risk of AS. The mTOR signaling pathway contributes to AS progression by regulating autophagy, cell senescence, immune response, and lipid metabolism. Various botanical drugs and their functional compounds have been found to exert anti- AS effects by modulating the activity of the mTOR signaling pathway. In this review, we summarize the pathogenesis of AS based on the mTOR signaling pathway from the aspects of immune response, autophagy, cell senescence, and lipid metabolism, and comb the recent advances in natural compounds from botanical drugs to inhibit the mTOR signaling pathway and delay AS development. This review will provide a new perspective on the mechanisms and precision treatments of AS.

show abstract

Autophagy enhanced by curcumin ameliorates inflammation in atherogenesis via the TFEB–P300–BRD4 axis

Cited by 46 publications

References 56 publications

Naringenin facilitates M2 macrophage polarization after myocardial ischemia–reperfusion by promoting nuclear translocation of transcription factor EB and inhibiting the NLRP3 inflammasome pathway

Naringenin facilitates M2 macrophage polarization after myocardial ischemia–reperfusion by promoting nuclear translocation of transcription factor EB and inhibiting the NLRP3 inflammasome pathway

New opportunities and challenges of natural products research: When target identification meets single-cell multiomics

Natural compounds from botanical drugs targeting mTOR signaling pathway as promising therapeutics for atherosclerosis: A review

Contact Info

Product

Resources

About