Ischemic Postconditioning-Mediated DJ-1 Activation Mitigate Intestinal Mucosa Injury Induced by Myocardial Ischemia Reperfusion in Rats Through Keap1/Nrf2 Pathway

Chen, Rong; Li, Wei; Qiu, Zhen; Zhou, Qin; Zhang, Yuan; Ding, Ke; Meng, Qingtao; Xia, Zhongyuan

doi:10.3389/fmolb.2021.655619

Cited by 8 publications

(6 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous research unveiled that m 6 A-modified oxidative stress facilitates myocardial ischemia/reperfusion damage ( 30 , 31 ). NRF2 and its cytoplasmic repressor KEAP1 act as the main regulators of oxidative stress ( 32 ). Key m 6 A regulators were observably linked with NFE2L2 and KEAP1 in AMI ( Figure 3C ).…”

Section: Resultsmentioning

confidence: 99%

Characterization of the m6A regulators’ landscape highlights the clinical significance of acute myocardial infarction

Chao,

Zhang,

Zhang

et al. 2024

Front. Immunol.

View full text Add to dashboard Cite

ObjectiveAcute myocardial infarction (AMI) is a severe cardiovascular disease that threatens human life and health globally. N6-methyladenosine (m6A) governs the fate of RNAs via m6A regulators. Nevertheless, how m6A regulators affect AMI remains to be deciphered. To solve this issue, an integrative analysis of m6A regulators in AMI was conducted.MethodsWe acquired transcriptome profiles (GSE59867, GSE48060) of peripheral blood samples from AMI patients and healthy controls. Key m6A regulators were used for LASSO, and consensus clustering was conducted. Next, the m6A score was also computed. Immune cell infiltration, ferroptosis, and oxidative stress were evaluated. In-vitro and in-vivo experiments were conducted to verify the role of the m6A regulator ALKBH5 in AMI.ResultsMost m6A regulators presented notable expression alterations in circulating cells of AMI patients versus those of controls. Based on key m6A regulators, we established a gene signature and a nomogram for AMI diagnosis and risk prediction. AMI patients were classified into three m6A clusters or gene clusters, respectively, and each cluster possessed the unique properties of m6A modification, immune cell infiltration, ferroptosis, and oxidative stress. Finally, the m6A score was utilized to quantify m6A modification patterns. Therapeutic targeting of ALKBH5 greatly alleviated apoptosis and intracellular ROS in H/R-induced H9C2 cells and NRCMs.ConclusionAltogether, our findings highlight the clinical significance of m6A regulators in the diagnosis and risk prediction of AMI and indicate the critical roles of m6A modification in the regulation of immune cell infiltration, ferroptosis, and oxidative stress.

show abstract

Section: Resultsmentioning

confidence: 99%

Characterization of the m6A regulators’ landscape highlights the clinical significance of acute myocardial infarction

Chao,

Zhang,

Zhang

et al. 2024

Front. Immunol.

View full text Add to dashboard Cite

show abstract

“…Ischemic post-conditioning has been shown to reduce IRI in several vital organs ( 5 , 34 , 35 ). It can protect the brain from IRI and improve neurological deficits through a variety of endogenous protective mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Cerebral protection by remote ischemic post-conditioning in patients with ischemic stroke: A systematic review and meta-analysis of randomized controlled trials

et al. 2022

View full text Add to dashboard Cite

BackgroundThere is evidence that remote limb ischemic postconditioning (RIPostC) can reduce ischemia-reperfusion injury (IRI) and improve the prognosis of patients with ischemic stroke. However, so far, only few relevant clinical studies have been conducted. Therefore, we carried out a meta-analysis of eligible randomized controlled trials to compare the RIPostC group with a control group (no intervention or sham surgery) in patients with ischemic stroke.MethodsFour English-language publication databases, PubMed, Cochrane, Embase, and Web of Science, were systematically searched up to March 2022. The data were analyzed using Review Manager fixed-effects and random-effects models.ResultsA total of 12 studies were included, and 11 of those were analyzed quantitatively. Compared to controls, The RIPostC group showed significantly reduced NIHHS scores in patients with ischemic stroke, (MD: −1.09, 95% confidence interval [CI]: −1.60, −0.57, P < 0.0001) and improved patients' Montreal Cognitive Assessment (MoCA) scores, (MD: 1.89, 95% CI: 0.78, 3.00, P = 0.0009), Our results showed that RIPostC is safe, (RR = 0.81, 95%CI: 0.61, 1.08, P = 0.15).ConclusionOur meta-analysis showed that RIPostC is safe and effective and has a positive cerebral protective effect in patients with ischemic stroke, which is safe and effective, and future large-sample, multicenter trials are needed to validate the cerebral protective effect of RIPostC.

show abstract

“…Nrf2, NQO1, and HO-1, as antioxidative molecules, were always used as biomarkers to detect the drug effects on MI and Parkinson’s disease ( 36 , 37 ), for instance, cytoplasm HO-1, cytoplasm NQO1, and nucleus Nrf2 expressions increased both in vivo and in vitro using azafrin after MI. Ischemic postconditioning increased the expression of Nrf2, NQO1, and HO-1 and impeded MI-induced oxidative stress ( 38 ). The NOS3 c.894G > T and 27-bp VNTR polymorphisms can be used for CAD screening ( 39 ).…”

Section: Discussionmentioning

confidence: 99%

Ferroptosis and Autophagy-Related Genes in the Pathogenesis of Ischemic Cardiomyopathy

Zheng

Gao

Zhang

et al. 2022

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

BackgroundObesity plays an important role in type 2 diabetes mellitus (T2DM) and myocardial infarction (MI). Ferroptosis and ferritinophagy are related to metabolic pathways, such as fatty acid metabolism and mitochondrial respiration. We aimed to investigate the ferroptosis- and autophagy-related differentially expressed genes (DEGs) that might be potential targets for MI progression.MethodsGSE116250 was analyzed to obtain DEGs. A Venn diagram was used to obtain the overlapping ferroptosis- and autophagy-related DEGs. The enrichment pathway analysis was performed and the hub genes were obtained. Pivotal miRNAs, transcription factors, and drugs with the hub genes interactions were also predicted. The MI mice model was constructed, and qPCR analysis and single-cell sequencing were used to validate the hub genes.ResultsUtilizing the limma package and the Venn diagram, 26 ferroptosis-related and 29 autophagy-related DEGs were obtained. The list of ferroptosis-related DEGs was analyzed, which were involved in the cellular response to a toxic substance, cellular oxidant detoxification, and the IL-17 signaling pathway. The list of autophagy-related DEGs was involved in the regulation of autophagy, the regulation of JAK-STAT signaling pathway, and the regulation of MAPK cascade. In the protein-protein interaction network, the hub DEGs, such as IL-6, PTGS2, JUN, NQO1, NOS3, LEPR, NAMPT, CDKN2A, CDKN1A, and Snai1, were obtained. After validation using qPCR analysis in the MI mice model and single-cell sequencing, the 10 hub genes can be the potential targets for MI deterioration.ConclusionThe screened hub genes, IL-6, PTGS2, JUN, NQO1, NOS3, LEPR, NAMPT, CDKN2A, CDKN1A, and Snai1, may be therapeutic targets for patients with MI and may prevent adverse cardiovascular events.

show abstract

Ischemic Postconditioning-Mediated DJ-1 Activation Mitigate Intestinal Mucosa Injury Induced by Myocardial Ischemia Reperfusion in Rats Through Keap1/Nrf2 Pathway

Cited by 8 publications

References 57 publications

Characterization of the m6A regulators’ landscape highlights the clinical significance of acute myocardial infarction

Characterization of the m6A regulators’ landscape highlights the clinical significance of acute myocardial infarction

Cerebral protection by remote ischemic post-conditioning in patients with ischemic stroke: A systematic review and meta-analysis of randomized controlled trials

Ferroptosis and Autophagy-Related Genes in the Pathogenesis of Ischemic Cardiomyopathy

Contact Info

Product

Resources

About