The effect of perceived stress on binge eating behavior among Chinese university students: a moderated mediation model.

Introduction: Previous studies have demonstrated a strong link between perceived stress and binge eating behavior, but the psychological mechanisms underlying such phenomenon are not fully understood. The present study further addressed this issue in a life history framework, focusing on life history strategy and distress tolerance. Methods: Firstly, we investigated the mediation role of life history strategy on the relationship between perceived stress and binge eating behavior. Secondly, we examined the moderation role of distress tolerance on the effect of perceived stress on life history strategy, as well as on the direct effect of perceived stress on binge eating behavior. We analyzed data from 1342 Chinese university students. Results: Results indicated that life history strategy mediates the relationship between perceived stress and binge eating behavior; distress tolerance has significant moderating effects on the direct effect of perceived stress on binge eating behavior and their indirect effect via life history strategy. Discussion: Therefore, distress tolerance skills training and life history-based interventions might be potentially effective ways to reduce binge eating behavior triggered by perceived stress.

Inhibition of SIRT1 in the nucleus accumbens attenuates heroin addiction-related behavior by decreasing D1 neuronal autophagy.

This study aimed to investigate the effects of SIRT1 modulation on heroin addiction-like behavior and its possible biological mechanisms. Wild-type C57BL/6J and Sirt1loxp/loxp D1-Cre mice were used in this experiment, and Sirt1 loxp/loxp D1-Cre(-) mice were used as a control for conditional knockout mice. Mice were divided into saline control and heroin-dependent groups. Behavioral methods were used to record the withdrawal response, conditioned place preference (CPP) changes, and open field test results. Transmission electron microscopy (TEM) was used to observe the structure of autophagosomes in nucleus accumbens (NAc) neurons. The expression of SIRT1 and autophagy-related proteins and genes, such as LC3Ⅱ, ATG5 , and ATG7 , was detected in the NAc of each mouse group via western blot, real-time quantitative PCR (qPCR) analyzes, and immunofluorescence. The results of this experiment showed that compared with the saline group, mice in the wild-type heroin-dependent group showed marked withdrawal symptoms, with more autophagosomes observed in NAc via TEM. Compared with wild-type and Sirt1loxp/loxp D1-Cre(-) heroin-dependent groups, CPP formation was found to be reduced in the conditional knockout mouse group, with a significant decrease in spontaneous activity. Western blot, qPCR, and immunofluorescence results indicated that the expression of LC3Ⅱ, ATG-5, and ATG-7 was significantly reduced in the NAc of the Sirt1loxp/loxp D1-Cre(+) group. It was still, however, higher than that in the saline control group. These results suggest that inhibition of Sirt1 expression may prevent heroin-induced addiction-related behaviors via reducing D1 neuronal autophagy.

A novel role for the ROS-ATM-Chk2 axis mediated metabolic and cell cycle reprogramming in the M1 macrophage polarization.

Reactive oxygen species (ROS) play a pivotal role in macrophage-mediated acute inflammation. However, the precise molecular mechanism by which ROS regulate macrophage polarization remains unclear. Here, we show that ROS function as signaling molecules that regulate M1 macrophage polarization through ataxia-telangiectasia mutated (ATM) and cell cycle checkpoint kinase 2 (Chk2), vital effector kinases in the DNA damage response (DDR) signaling pathway. We further demonstrate that Chk2 phosphorylates PKM2 at the T95 and T195 sites, promoting glycolysis and facilitating macrophage M1 polarization. In addition, Chk2 activation increases the Chk2-dependent expression of p21, inducing cell cycle arrest for subsequent macrophage M1 polarization. Finally, Chk2-deficient mice infected with lipopolysaccharides (LPS) display a significant decrease in lung inflammation and M1 macrophage counts. Taken together, these results suggest that inhibiting the ROS-Chk2 axis can prevent the excessive inflammatory activation of macrophages, and this pathway can be targeted to develop a novel therapy for inflammation-associated diseases and expand our understanding of the pathophysiological functions of DDR in innate immunity.

Regulated secretion of mutant p53 negatively affects T lymphocytes in the tumor microenvironment.

Several studies have demonstrated the role of the oncogenic mutant p53 in promoting tumor progression; however, there is limited information on the effects of secreted oncogenic mutant p53 on the tumor microenvironment and tumor immune escape. In this study, we found that secretion of mutant p53, determined by exosome content, is dependent on its N-terminal dileucine motif via its binding to ß-adaptin, and inhibited by the CHK2-mediated-Ser 20 phosphorylation. Moreover, we observed that the mutant p53 caused downregulation and dysfunction of CD4+ T lymphocytes in vivo and downregulated the levels and activities of rate-limiting glycolytic enzymes in vitro. Furthermore, inhibition of mutant p53 secretion by knocking down AP1B1 or mutation of dileucine motif could reverse the quantity and function of CD4+ T lymphocytes and restrain the tumor growth. Our study demonstrates that the tumor-derived exosome-mediated secretion of oncogenic mutant p53 inhibits glycolysis to alter the immune microenvironment via functional suppression of CD4+ T cells, which may be the underlying mechanism for tumor immune escape. Therefore, targeting TDE-mediated p53 secretion may serve as a potential therapeutic target for cancer treatment.

Atg7 senses ATP levels and regulates AKT1-PDCD4 phosphorylation-ubiquitination axis to promote survival during metabolic stress.

We report that autophagy-related gene 7 (ATG7) modulates p53 activity to regulate cell cycle and survival during metabolic stress, and that indicates Atg7 is functionally involved in cellular homeostasis in autophagy independent fashion. As a protein translation inhibitor, Programmed cell death 4 (PDCD4) expression is regulated by AKT1 phosphorylation. Here, we find that Atg7 interacts with PDCD4 and AKT1 to regulate AKT1-PDCD4 phosphorylation-ubiquitination axis during metabolic stress. We demonstrate that Atg7 senses decrease of ATP levels to suppress AKT-mediated PDCD4 phosphorylation at Ser67, which inhibits PDCD4 ubiquitinating during metabolic stress. Finally, PDCD4 accumulates and functions as a protein translation inhibitor to conserve energy, thus reducing apoptosis and allowing cells to survive stress periods. These results suggest that the ATP-Atg7-PDCD4 axis acts as a metabolic adaptation pathway which dictates cells to overcome metabolic stress.

The effect of gender in binge eating behavior in Chinese culture: the serial mediation model of body dissatisfaction and self-acceptance.

Introduction: The gender difference of binge eating behavior been highlighted by previous studies. However, psychological mechanisms underlying the gender difference of binge eating behavior remain unclear. This study addressed this issue from a sociocultural perspective. Methods: Firstly, we investigated the mediation effect of body dissatisfaction on the gender difference of binge eating behavior. Secondly, we examine the serial mediating role of body dissatisfaction and self-acceptance in gender differences of binge eating behavior. Here, we analyzed data from 703 Chinese university students using SPSS 26.0 and SPSS PROCESS. Results: In Chinese culture, body dissatisfaction and self-acceptance independently or through a serial way mediate the gender differences in binge eating behaviors. Discussion: We discussed the implications and limitations of the present study.

A modified behavioral test protocol for simultaneously evaluating the incentive value of alcohol drinking and social interaction in mice.

Individual sociability and alcohol drinking are interacted to escalate alcohol use. An impairment in perceiving and discriminating the difference in incentive values between social interaction and drinking behavior indicates a shift from moderate alcohol consumption to misuse. However, few studies have evaluated the incentive value of these two behaviors in the same scenario. Thus, we modified a behavioral test protocol to evaluate rodents' ability to perceive and discriminate the differences in incentive value between alcohol drinking and interaction with their social partners. The present protocol is simple and practicable. Only 2-3 days are required to complete the whole process. Compared with existing methods, our protocol is simple and practicable. Our findings suggested that subtle changes in the incentive value of distinct behaviors can be accurately and reliably assessed using the present protocol in mice with low or high levels of alcohol preference.•We described a modified behavioral test protocol to simultaneously evaluate the incentive value of alcohol drinking and social interaction.•The subtle changes in the incentive value of mice with different levels of alcohol preference can be accurately and reliably assessed in the present protocol.•Using our modified protocol, the differences of incentive value between distinct behaviors can be accurately and reliably assessed in mice with different risks to develop into AUD.

Radiotherapy dosimetry and radiotherapy related complications of immediate implant-based reconstruction after breast cancer surgery.

Backgrounds: The impact of immediate implant-based breast reconstruction (IBBR) on the delivery of radiotherapy plans remains controversial. This study aimed to compare the differences in radiotherapy dosimetry, complications of radiotherapy, and quality of life in patients who underwent modified radical mastectomy combined with or without IBBR. Methods: We retrospectively collected 104 patients with breast cancer who underwent intensity-modulated radiation therapy after modified radical mastectomy with IBBR (n =46) or not (n =58) from January 2017 to December 2021. The dosimetric differences in radiotherapy of planning target volume (PTV) and organs at risk and the differences in complications of radiotherapy between the two groups were compared. We also applied the functional assessment of cancer therapy-breast cancer (FACT-B) score to compare the difference in quality of life. The chi-square test and independent samples t-test were used to analyze the above data. Results: IBBR group was associated with higher PTV volumes, PTV D98, V95, and lower PTV Dmean, D2 compared with the non-reconstruction group (P<0.05). IBBR group also had lower radiotherapy dosimetric parameters in the ipsilateral lung and the heart of left breast cancer patients. The differences in the rates of radiation pneumonia (RP) and radiation dermatitis (RD) between the two groups were not statistically significant (P > 0.05). Moreover, FACT-B scores at 6 months after radiotherapy in patients with IBBR were higher than those without reconstruction (P < 0.05). Conclusion: Patients with IBBR achieved better radiation dosimetry distribution and higher quality of life without more complications of radiotherapy.

De-ubiquitination of SAMHD1 by USP7 promotes DNA damage repair to overcome oncogenic stress and affect chemotherapy sensitivity.

Oncogenic stress induces DNA damage repair (DDR) that permits escape from mitotic catastrophe and allows early precursor lesions during the evolution of cancer. SAMHD1, a dNTPase protecting cells from viral infections, has been recently found to participate in DNA damage repair process. However, its role in tumorigenesis remains largely unknown. Here, we show that SAMHD1 is up-regulated in early-stage human carcinoma tissues and cell lines under oxidative stress or genotoxic insults. We further demonstrate that de-ubiquitinating enzyme USP7 interacts with SAMHD1 and de-ubiquitinates it at lysine 421, thus stabilizing SAMHD1 protein expression for further interaction with CtIP for DDR, which promotes tumor cell survival under genotoxic stress. Furthermore, SAMHD1 levels positively correlates with USP7 in various human carcinomas, and is associated with an unfavorable survival outcome in patients who underwent chemotherapy. Moreover, USP7 inhibitor sensitizes tumor cells to chemotherapeutic agents by decreasing SAMHD1 in vitro and in vivo. These findings suggest that de-ubiquitination of SAMHD1 by USP7 promotes DDR to overcome oncogenic stress and affect chemotherapy sensitivity.

The effect of mindfulness on social media addiction among Chinese college students: A serial mediation model.

Introduction: The COVID-19 pandemic has exacerbated social media addiction (SMA), making it urgent to find effective interventions for social media addiction. Evidence has shown that mindfulness might be an effective intervention for social media addiction. However, psychological mechanisms by which mindfulness reduce social media use remain unclear. Here, we further addressed this issue to examine whether attentional control and fear of missing out (FOMO) mediate the relationship between mindfulness and SMA. Methods: We recruited 446 college students from two universities in China and analyzed the data. Results: The results suggest that there are mediation effects of attentional control and FOMO between mindfulness and SMA through 3 paths: path 1, mindfulness → attention control → SMA (-0.04); path 2, mindfulness → FOMO → SMA (-0.22); and path 3, mindfulness → attention control → FOMO → SMA (-0.05). Discussion: Therefore, mindfulness-based interventions may be an effective way to alleviate social media addiction, especially mindfulness-based interventions targeting FOMO. At the end of the article, we also discussed the limitations of this study.

Effect of body dissatisfaction on binge eating behavior of Chinese university students: A moderated mediation model.

The relationship between body dissatisfaction and binge eating behavior has been highlighted by previous studies. However, the psychological mechanisms underlying body dissatisfaction-induced binge eating behavior remain unclear. Here, we further addressed this issue in the framework of the sociocultural model of eating disorders. Firstly, we investigated the mediation effect of perceived stress on the relationship between body dissatisfaction and binge eating. Secondly, we examined the moderation role of the self-acceptance and emotion regulation strategies on the indirect effect of body dissatisfaction on binge eating behavior mediated by perceived stress. Data from 903 Chinese university students were analyzed using SPSS 26.0 and SPSS PROCESS Macro. Results indicated that perceived stress mediates the relationship between body dissatisfaction and binge eating behavior. Main interactional effects have been observed when self-acceptance and cognitive reappraisal but not expressive suppression are introduced in the model as a moderator. Implications and limitations of the study are discussed.

Diet-induced inflammation in the anterior paraventricular thalamus induces compulsive sucrose-seeking.

Overconsumption of palatable food may initiate neuroadaptive responses in brain reward circuitry that may contribute to eating disorders. Here we report that high-fat diet (HFD) consumption impedes threat-cue-induced suppression of sucrose-seeking in mice. This compulsive sucrose-seeking was due to enhanced cue-triggered neuronal activity in the anterior paraventricular thalamus (aPVT) resulting from HFD-induced microglia activation. Thus, metabolic inflammation in the aPVT produces an adaptive response to threat cues, leading to compulsive food-seeking.

Efficacy and Safety of Non-Steroidal Mineralocorticoid Receptor Antagonists in Patients With Chronic Kidney Disease and Type 2 Diabetes: A Systematic Review Incorporating an Indirect Comparisons Meta-Analysis.

Background: The non-steroidal mineralocorticoid receptor antagonists (MRAs) are promising treatments in patients with chronic kidney disease (CKD) and type 2 diabetes (T2D). We conducted a meta-analysis to explore the efficacy and safety of the non-steroidal MRAs (finerenone, apararenone, esaxerenone) and detect the differences among them. Methods: We searched several databases for eligible randomized controlled trials (RCTs) investigating non-steroidal MRAs versus placebo in patients with CKD and T2D. We performed a conventional meta-analysis separately, and then indirect comparisons for efficacy and safety outcomes were conducted among these included drugs. Results: Eight RCTs with 14,450 subjects were enrolled. In patients with CKD and T2D, a greater reduction in urinary albumin-to-creatinine ratio (UACR) (WMD -0.40, 95% CI -0.48 to -0.32, p < 0.001), estimated glomerular filtration rate (eGFR) (WMD -2.69, 95% CI -4.47 to -0.91, p = 0.003), systolic blood pressure (SBP) (WMD -4.84, 95% CI -5.96 to -3.72, p < 0.001) and a higher risk of hyperkalemia (RR 2.07, 95% CI 1.86 to 2.30, p < 0.001) were observed in the non-steroidal MRAs versus placebo; there is no significant difference in the incidence of serious adverse events between two groups (RR 1.32, 95% CI 0.98 to 1.79, p = 0.067). Compared with finerenone, esaxerenone showed no significant difference in UACR reduction (WMD 0.24, 95% CI -0.016 to 0.496, p = 0.869); apararenone and esaxerenone showed greater decreases in SBP (WMD 1.37, 95% CI 0.456 to 2.284, p = 0.010; WMD 3.11, 95% CI 0.544 to 5,676, p = 0.021). Conclusions: Despite the moderate increased risk of hyperkalemia, use of non-steroidal MRAs could reduce proteinuria and SBP in patients with CKD and T2D. In terms of renoprotection, esaxerenone and finerenone may have similar effects. Esaxerenone and apararenone may have better antihypertensive effects than finerenone. The head-to-head RCTs are still needed to compare the differences of the efficacy and safety in these non-steroidal MRAs.

Effect of Self-Efficacy on Bedtime Procrastination Among Chinese University Students: A Moderation and Mediation Model.

Bedtime procrastination (BP) is generally considered to be a maladaptive behavior. However, BP may be an adaptive fast LH strategy within the LH framework, and further, personal beliefs about their abilities and resources promote this fast LH strategy. Here, the present study addressed this idea, focusing on the effect of self-efficacy on BP, the mediation of harm avoidance (HA), and the moderation of novelty seeking (NS). Data from 552 Chinese university students (205 men and 347 women) were analyzed using SPSS 25.0 and SPSS PROCESS Macro. Results indicated that HA partially mediates the relationship between self-efficacy and BP. Main interactional effects have been observed when NS is introduced in the model as a moderator. Implications and limitations of the study and suggestions for further study are discussed.

The longitudinal effect of the atherogenic index of plasma on type 2 diabetes in middle-aged and older Chinese.

AIMS: Atherogenic Index of Plasma (AIP) has been proposed as a novel marker of plasma atherogenicity, but its longitudinal predictive value in type 2 diabetes mellitus (T2DM) remains unclear. We aimed to assess the associations of AIP and its longitudinal transition with T2DM among middle-aged and older Chinese. METHODS: Data were extracted from four rounds of the China Health and Retirement Longitudinal Study (2011, 2013, 2015, and 2018). AIP was calculated as log10 (triglyceride/high-density lipoprotein cholesterol). Participants were classified into high and low AIP groups at baseline, and subsequently into four transition patterns during follow-up: maintained-high, maintained-low, high-to-low, and low-to-high AIP. Multivariable Cox frailty models were applied to explore the longitudinal transition patterns of AIP on the development of T2DM. RESULTS: A total of 8760 subjects without T2DM were selected in 2011, of which 981 developed T2DM until 2018. When compared with people with maintained-low AIP patterns, those with transition patterns of maintained-high AIP, high-to-low AIP, and low-to-high AIP were at around 1.5 times higher risk of T2DM (HRadj = 1.69, 1.32, and 1.47, respectively, all P < 0.05). However, the risk of T2DM did not decrease in the high-to-low AIP group as compared to the maintained-high AIP group. CONCLUSIONS: Three longitudinal AIP transition patterns (maintained-high AIP, high-to-low AIP, and low-to-high AIP) were associated with the development of T2DM. Preventions are needed to combat T2DM at an early dyslipidemic stage.

Long noncoding RNA PTTG3P/miR-192-3p/CCNB1 axis is a potential biomarker of childhood asthma.

BACKGROUND: Increasing evidence suggests that long non-coding RNAs (lncRNAs) affect the regulation of immune responses, airway inflammation, and other pathological processes involved in asthma. LncRNA PTTG3P is associated with the development of various tumors, but its role in childhood asthma remains unknown. In this study, we investigated the functions of the lncRNA PTTG3P in the progression of childhood asthma. METHODS: Twenty-six healthy children and 26 asthmatic children were monitored for disease progression for 2 years. We obtained blood samples during the chronic phase of disease for lncRNA/mRNA expression microarray analysis. A competitive endogenous RNA network (PTTG3P/miR-192-3p/CCNB1) was identified using bioinformatics analyses. Real-time qPCR and western blot were used to quantify gene and protein expression levels, respectively. Cell counting kit­8 and transwell assays were used to evaluate the proliferation and migration of bronchial epithelial (16HBE) cells. Double luciferase reporter gene assay was used to validate the predictive targets in PTTG3P, miR-192-3p, and CCNB1. RESULTS: PTTG3P was highly expressed in the peripheral blood of asthmatic children. Knocking down PTTG3P inhibited epithelial-mesenchymal transition, proliferation, and migration of 16HBE cells. PTTG3P promoted progression of childhood asthma by targeting the miR-192-3p/CCNB1 axis. CONCLUSIONS: Childhood asthma was associated with the PTTG3P/miR-192-3p/CCNB1 axis. This study provides potential diagnostic and treatment biomarkers for childhood asthma.

Post-Translational Modifications of PCNA in Control of DNA Synthesis and DNA Damage Tolerance-the Implications in Carcinogenesis.

The faithful DNA replication is a critical event for cell survival and inheritance. However, exogenous or endogenous sources of damage challenge the accurate synthesis of DNA, which causes DNA lesions. The DNA lesions are obstacles for replication fork progression. However, the prolonged replication fork stalling leads to replication fork collapse, which may cause DNA double-strand breaks (DSB). In order to maintain genomic stability, eukaryotic cells evolve translesion synthesis (TLS) and template switching (TS) to resolve the replication stalling. Proliferating cell nuclear antigen (PCNA) trimer acts as a slide clamp and encircles DNA to orchestrate DNA synthesis and DNA damage tolerance (DDT). The post-translational modifications (PTMs) of PCNA regulate these functions to ensure the appropriate initiation and termination of replication and DDT. The aberrant regulation of PCNA PTMs will result in DSB, which causes mutagenesis and poor response to chemotherapy. Here, we review the roles of the PCNA PTMs in DNA duplication and DDT. We propose that clarifying the regulation of PCNA PTMs may provide insights into understanding the development of cancers.

Fructose-1,6-bisphosphatase aggravates oxidative stress-induced apoptosis in asthma by suppressing the Nrf2 pathway.

Asthma is a chronic airway disease that causes excessive inflammation, oxidative stress, mucus production and bronchial epithelial cell apoptosis. Fructose-1,6-bisphosphatase (Fbp1) is one of the rate-limiting enzymes in gluconeogenesis and plays a critical role in several cancers. However, its role in inflammatory diseases, such as asthma, is unclear. Here, we examined the expression, function and mechanism of action of Fbp1 in asthma. Gene Expression Omnibus (GEO) data sets revealed that Fbp1 was overexpressed in a murine model of asthma and in interleukin (IL)-4- or IL-13-stimulated bronchial epithelial cells. We confirmed the findings in an animal model as well as Beas-2B and 16HBE cells. In vitro investigations revealed that silencing of Fbp1 reduced apoptosis and the proportion of cells in the G2/M phase, whereas overexpression led to increases. Fbp1 knock-down inhibited oxidative stress by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, whereas Fbp1 overexpression aggravated oxidative stress by suppressingthe Nrf2 pathway. Moreover, the Nrf2 pathway inhibitor ML385 reversed the changes caused by Fbp1 inhibition in Beas-2B and 16HBE cells. Collectively, our data indicate that Fbp1 aggravates oxidative stress-induced apoptosis by suppressing Nrf2 signalling, substantiating its potential as a novel therapeutic target in asthma.

MicroRNA-370 carried by M2 macrophage-derived exosomes alleviates asthma progression through inhibiting the FGF1/MAPK/STAT1 axis.

Emerging evidence has suggested the functions of exosomes in allergic diseases including asthma. By using a mouse model with asthma induced by ovalbumin (OVA), we explored the roles of M2 macrophage-derived exosomes (M2Φ-Exos) in asthma progression. M2Φ-Exos significantly alleviated OVA-induced fibrosis and inflammatory responses in mouse lung tissues, as well as inhibited abnormal proliferation, invasion, and fibrosis-related protein production in platelet derived growth factor (PDGF-BB) treated primary mouse airway smooth muscle cells (ASMCs). The OVA administration in mice or the PDGF-BB treatment in ASMCs reduced the expression of miR-370, which was detected in M2Φ-Exos by miRNA sequencing. However, treating the mice or ASMCs with M2Φ-Exos reversed the inhibitory effect of OVA or PDGF-BB on miR-370 expression. We identified that the target of miR-370 was fibroblast growth factor 1 (FGF1). Downregulation of miR-370 by Lv-miR-370 inhibitor or overexpression of FGF1 by Lv-FGF1 blocked the protective roles of M2Φ-Exos in asthma-like mouse and cell models. M2Φ-Exos were found to inactivate the MAPK signaling pathway, which was recovered by miR-370 inhibition or FGF1 overexpression. Collectively, we conclude that M2Φ-Exos carry miR-370 to alleviate asthma progression through downregulating FGF1 expression and the MAPK/STAT1 signaling pathway. Our study may offer a novel insight into asthma treatment.

Significance of RNA N6-Methyladenosine Regulators in the Diagnosis and Subtype Classification of Childhood Asthma Using the Gene Expression Omnibus Database.

RNA N6-methyladenosine (m6A) regulators play important roles in a variety of biological functions. Nonetheless, the roles of m6A regulators in childhood asthma remain unknown. In this study, 11 significant m6A regulators were selected using difference analysis between non-asthmatic and asthmatic patients from the Gene Expression Omnibus GSE40888 dataset. The random forest model was used to screen five candidate m6A regulators (fragile X mental retardation 1, KIAA1429, Wilm's tumor 1-associated protein, YTH domain-containing 2, and zinc finger CCCH domain-containing protein 13) to predict the risk of childhood asthma. A nomogram model was established based on the five candidate m6A regulators. Decision curve analysis indicated that patients could benefit from the nomogram model. The consensus clustering method was performed to differentiate children with asthma into two m6A patterns (clusterA and clusterB) based on the selected significant m6A regulators. Principal component analysis algorithms were constructed to calculate the m6A score for each sample to quantify the m6A patterns. The patients in clusterB had higher m6A scores than those in clusterA. Furthermore, we found that the patients in clusterA were linked to helper T cell type 1 (Th1)-dominant immunity while those in clusterB were linked to Th2-dominant immunity. In summary, m6A regulators play nonnegligible roles in the occurrence of childhood asthma. Our investigation of m6A patterns may be able to guide future immunotherapy strategies for childhood asthma.