Functional mechanism of AMPK activation in mitochondrial regeneration of rat peritoneal macrophages mediated by uremic serum

Chen, De; Zuo, Kun; Liang, Xuan; Wang, Mei; Zhang, Honghong; Zhou, Rong; Liu, Xiaoli

doi:10.1371/journal.pone.0235960

Cited by 6 publications

(8 citation statements)

References 22 publications

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“…Specifically, the overall concept, objectives, study design, and methodology of this article [ 1 ] are similar to work reported in previously published Master’s theses [ 2 , 3 ] and a published article [ 4 ]. The experimental design and results reported in all figures and tables of [ 1 ] appear very similar to those previously reported in [ 2 , 3 ], though the individual data values reported are not identical.…”

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confidence: 70%

“…After this article [ 1 ] was published, concerns were raised regarding the similarity to previous works [ 2 – 4 ] by different authors and that were not cited in [ 1 ].…”

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confidence: 99%

“…Overall, the comments and data received from the author did not resolve PLOS’ concerns about the data provided for [ 1 ] and the high degree of similarity between the research reported in [ 1 ] and [ 2 – 4 ].…”

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confidence: 99%

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Retraction: Functional mechanism of AMPK activation in mitochondrial regeneration of rat peritoneal macrophages mediated by uremic serum

2024

PLoS ONE

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confidence: 70%

“…After this article [ 1 ] was published, concerns were raised regarding the similarity to previous works [ 2 – 4 ] by different authors and that were not cited in [ 1 ].…”

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confidence: 99%

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Retraction: Functional mechanism of AMPK activation in mitochondrial regeneration of rat peritoneal macrophages mediated by uremic serum

2024

PLoS ONE

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“…The heatmap was analyzed using an online server Heatmapper ( www.heatmapper.ca/expression/ ). Rat peritoneal macrophages (RPMs) were isolated and cultured as described previously ( Chen et al, 2020 ). RPMs grown in 12-well plates (5 × 10 5 cells/well) were treated by LPS (10 ng/mL) plus soluble cholesterol (CHO; 100 μg/mL) with or without the presence of Art (20 μg/mL) for 1 h ( n = 5).…”

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confidence: 99%

Anti-malarial artesunate ameliorates atherosclerosis by modulating arterial inflammatory responses via inhibiting the NF-κB–NLRP3 inflammasome pathway

et al. 2023

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Introduction: Chronic inflammation plays a critical role in the pathogenesis of atherosclerosis (AS), and involves a complex interplay between blood components, macrophages, and arterial wall. Therefore, it is valuable in the development of targeted therapies to treat AS.Methods: AS rat model was induced by atherogenic diet plus with lipopolysaccharide (LPS) and then treated by anti-malarial artesunate (Art), a succinate derivative of artemisinin. The arterial morphology was observed after Oil red O, hematoxylin—eosin, and Masson’s staining. The arterial protein level was detected by immunohistochemistry or immunofluorescence. The expression level of mRNA was determined by PCR array or real-time PCR.Results: Herein, we showed that Art possessed a dose-dependently protective effect on AS rats. In detail, Art showed a comparable inhibitory effect on arterial plaque and serum lipids compared to those of rosuvastatin (RS), and further showed a better inhibition on arterial lipid deposition and arterial remodeling comprised of arterial wall thicken and vascular collagen deposition, than those of RS. The improvement of Art on AS rats was related to inhibit arterial macrophage recruitment, and inhibit nuclear factor κB (NF-κB)-related excessive arterial inflammatory responses. Critically, Art showed significant inhibition on the NLRP3 inflammasome activation in both arterial wall and arterial macrophages, by down-regulating the expression of NOD-like receptor thermal protein domain associated protein 3 (NLRP3) and apoptosis associated speckle-like protein containing CARD (ASC), leading to less production of the NLRP3 inflammasome—derived caspase-1, interleukin-1β (IL-1β), IL-18, and subsequent transforming growth factor β1 (TGF-β1) in AS rats.Conclusion: We propose that Art is an anti-AS agent acts through modulating the arterial inflammatory responses via inhibiting the NF-κB – NLRP3 inflammasome pathway.

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“…Rat peritoneal macrophages (PMs) were isolated as described previously [47]. In brief, animals were intraperitoneally injected with ice-cold PBS and peritoneal fluid was aspirated and centrifuged at 300 g for 5 min.…”

Section: Peritoneal Macrophage Culturementioning

confidence: 99%

Propofol ameliorates renal ischemia/reperfusion injury by enhancing macrophage M2 polarization through PPARγ/STAT3 signaling

Liu

Meng

Miao

et al. 2021

Aging

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Propofol (Pro) confers protection against renal ischemia/reperfusion (rI/R) injury through incompletely characterized mechanisms. Since Pro has shown net anti-inflammatory properties as part of its beneficial effects, we examined the potential role of Pro in the modulation of macrophage polarization status during both rI/R injury in vivo and exposure of cultured peritoneal macrophages (PMs) to hypoxia/reoxygenation (H/R). Rats were subjected to 45-min r/IR surgery or a sham procedure and administered PBS (vehicle) or Pro during the ischemia stage. Pro administration attenuated rI/R-induced kidney damage and renal TNF-α, IL-6, and CXCL-10 expression. Enhanced macrophage M2 polarization, evidenced by reduced iNOS and increased Arg1 and Mrc1 mRNA levels, was further detected after Pro treatment both in the kidney, after rI/R in vivo, and in H/R-treated PMs. Pro administration also repressed phosphorylated signal transducer and activator of transcription 1 (p-STAT1) and increased p-STAT3, p-STAT6, and peroxisome proliferatoractivated receptor-γ (PPARγ) mRNA levels in H/R-exposed PMs. Importantly, siRNA-mediated PPARγ silencing repressed Pro-mediated STAT3 activation in PMs and restored proinflammatory cytokine levels and prevented macrophage M2 marker expression in both rI/R-treated rats and cultured PMs. These findings suggest that Pro confers renoprotection against rI/R by stimulating PPARγ/STAT3-dependent macrophage conversion to the M2 phenotype.

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Functional mechanism of AMPK activation in mitochondrial regeneration of rat peritoneal macrophages mediated by uremic serum

Abstract: Objective To investigate the effects of AMPK activation on mitochondrial inhibition by uremic serum through the AMPK-activated rat peritoneal macrophages stimulated by uremic serum, thereby providing a reference for the clinical treatment of chronic kidney disease.

Cited by 6 publications

References 22 publications

Retraction: Functional mechanism of AMPK activation in mitochondrial regeneration of rat peritoneal macrophages mediated by uremic serum

Retraction: Functional mechanism of AMPK activation in mitochondrial regeneration of rat peritoneal macrophages mediated by uremic serum

Anti-malarial artesunate ameliorates atherosclerosis by modulating arterial inflammatory responses via inhibiting the NF-κB–NLRP3 inflammasome pathway

Propofol ameliorates renal ischemia/reperfusion injury by enhancing macrophage M2 polarization through PPARγ/STAT3 signaling

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