IL‐22‐mediated renal metabolic reprogramming via PFKFB3 to treat kidney injury

Chen, Wei; Shen, Yilan; Fan, Jiajun; Zeng, Xian; Zhang, Xu-Yao; Luan, Jingyun; Wang, Yichen; Zhang, Jinghui; Si, Fang; Mei, Xiaobin; Zhao, Zhen; Ju, Dianwen

doi:10.1002/ctm2.324

Cited by 21 publications

(22 citation statements)

References 46 publications

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“…Moreover, research suggests that MCL mitigates the severity of liver steatosis by enhancing autophagy and attenuating NF-κB-mediated inflammation ( Zhong et al, 2018 ). Additionally, it has been reported that resveratrol can inhibit the activation of the NLRP3 inflammasome by inducing autophagy, which ameliorates IgA nephropathy ( Wu et al, 2020 ; Chen et al, 2021 ). Considering this evidence, we speculated that MCL may alleviate radiation-induced pyroptosis by promoting autophagy and subsequently inhibiting the activation of the NLRP3 inflammasome.…”

Section: Discussionmentioning

confidence: 99%

Autophagy Induced by Micheliolide Alleviates Acute Irradiation-Induced Intestinal Injury via Inhibition of the NLRP3 Inflammasome

Shen

Jin

et al. 2022

Front. Pharmacol.

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Radiation-induced enteropathy (RIE) is one of the most common and fatal complications of abdominal radiotherapy, with no effective interventions available. Pyroptosis, a form of proinflammatory regulated cell death, was recently found to play a vital role in radiation-induced inflammation and may represent a novel therapeutic target for RIE. To investigate this, we found that micheliolide (MCL) exerted anti-radiation effects in vitro. Therefore, we investigated both the therapeutic effects of MCL in RIE and the possible mechanisms by which it may be therapeutic. We developed a mouse model of RIE by exposing C57BL/6J mice to abdominal irradiation. MCL treatment significantly ameliorated radiation-induced intestinal tissue damage, inflammatory cell infiltration, and proinflammatory cytokine release. In agreement with these observations, the beneficial effects of MCL treatment in RIE were abolished in Becn1+/− mice. Furthermore, super-resolution microscopy revealed a close association between NLR pyrin domain three and lysosome-associated membrane protein/light chain 3-positive vesicles following MCL treatment, suggesting that MCL facilitates phagocytosis of the NLR pyrin domain three inflammasome. In summary, MCL-mediated induction of autophagy can ameliorate RIE by NLR pyrin domain three inflammasome degradation and identify MCL as a novel therapy for RIE.

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Section: Discussionmentioning

confidence: 99%

Autophagy Induced by Micheliolide Alleviates Acute Irradiation-Induced Intestinal Injury via Inhibition of the NLRP3 Inflammasome

Shen

Jin

et al. 2022

Front. Pharmacol.

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“…Moreover, according to the safety evaluations tests, the rapid DNA vaccination strategy showed an excellent safety. Chen et al found that the immune system, including IL-22, was closely related to the recovery of kidney and liver (46)(47)(48). These results inspire us that DNA cancer vaccine is an effect cancer treatment with good safety.…”

Section: Discussionmentioning

confidence: 95%

Fast DNA Vaccination Strategy Elicits a Stronger Immune Response Dependent on CD8+CD11c+ Cell Accumulation

et al. 2021

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Conventional DNA vaccine strategies usually employ a regimen of immunizations at 2-week or longer intervals to induce effective memory cell-dependent immune responses. Clinical cancer treatment requires a faster immunization strategy to contend with tumor progression. In this study, a novel fast immunization strategy was established, wherein a DNA vaccine was intramuscularly administered on days 0, 2, and 5 in a murine lung cancer model. Effector cells peaked 7 to 10 days after the last vaccination. Compared with traditional 2-week-interval immunization strategies, antigen-specific cytolysis and INF-γ secretion were significantly enhanced under the fast vaccination approach. As a result, the rapidly administered DNA vaccine elicited stronger and more prompt antitumor effects. The probable underlying mechanism of fast immunization was the accumulation of CD8+CD11c+ antigen-presenting cells at the injection site, which enhanced subsequent antigen presentation. In conclusion, the fast DNA vaccination strategy shortened vaccination time to 5 days and elicited a stronger antitumor immune response.

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“…APAP-induced acute liver injury induces the expression of proinflammatory factors (such as IL-1β, IL-6, and TNF-α), which can then exacerbate organ damage, especially cause hepatocyte injury to damage the liver (Chen et al, 2020;Raevens et al, 2020;Saad et al, 2020;Chen et al, 2021). Therefore, inflammatory response is considered one of the basic mechanisms of APAP-induced liver injury (Huang et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Atractylenolide I Ameliorates Acetaminophen-Induced Acute Liver Injury via the TLR4/MAPKs/NF-κB Signaling Pathways

Lai

et al. 2022

Front. Pharmacol.

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Background: Acetaminophen (APAP) overdose results in the production of reactive oxygen species (ROS), induces hepatocyte necrosis, and leads to acute liver failure. Atractylenolide I (AO-I), a phytochemical found in Atractylodes macrocephala Koidz, is known to exhibit antioxidant activity. However, its clinical benefits against drug-induced liver injury remain largely unclear.Purpose: This study aimed at evaluating the protective effects of AO-I against APAP-induced acute liver injury.Methods: C57BL/6 mice were administered 500 mg/kg APAP to induce hepatotoxicity. AO-Ⅰ (60 and 120 mg/kg) was intragastrically administered 2 h before APAP dosing. Liver histopathological changes, oxidative stress and hepatic inflammation markers from each group were observed.Results: We observed that AO-I treatment significantly reversed APAP-induced liver injury, as evidenced by improved plasma alanine transaminase (ALT) level, aspartate aminotransferase (AST) and liver H&E stain. APAP treatment increased liver malondialdehyde (MDA) content and reduced catalase (CAT) and glutathione (GSH) level; however, these effects were alleviated by AO-I intervention. Moreover, AO-I treatment significantly inhibited APAP-induced activation of pro-inflammatory factors, such as IL-1β, IL-6, and TNF-α, at both the mRNA and protein levels. Mechanistic studies revealed that AO-I attenuated APAP-induced activation of TLR4, NF-κB and MAPKs (including JNK and p38).Conclusion: AO-I mediates protective effects against APAP-induced hepatotoxicity via the TLR4/MAPKs/NF-κB pathways. Thus, AO-I is a candidate therapeutic compound for APAP-induced hepatotoxicity.

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IL‐22‐mediated renal metabolic reprogramming via PFKFB3 to treat kidney injury

Cited by 21 publications

References 46 publications

Autophagy Induced by Micheliolide Alleviates Acute Irradiation-Induced Intestinal Injury via Inhibition of the NLRP3 Inflammasome

Autophagy Induced by Micheliolide Alleviates Acute Irradiation-Induced Intestinal Injury via Inhibition of the NLRP3 Inflammasome

Fast DNA Vaccination Strategy Elicits a Stronger Immune Response Dependent on CD8+CD11c+ Cell Accumulation

Atractylenolide I Ameliorates Acetaminophen-Induced Acute Liver Injury via the TLR4/MAPKs/NF-κB Signaling Pathways

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