Search Results (725)

Semantic segmentation of building facade images has enabled a lot of intelligent support for architectural research and practice in the last decade. However, the classifiers for semantic segmentation usually predict facade elements (e.g., windows) as graphics in irregular shapes. The non-smooth edges and hard-to-define shapes impede the further use of the predicted graphics. This study proposes a method to regularize the predicted graphics following the prior knowledge of composition principles of building facades. Specifically, we define four types of boxes for each predicted graphic, namely minimum circumscribed box (MCB), maximum inscribed box (MIB), candidate box (CB), and best overlapping box (BOB). Based on these boxes, a three-stage process, consisting of denoising, BOB finding, and BOB stacking, was established to regularize the predicted graphics of facade elements into basic rectilinear polygons. To compare the proposed and existing methods of graphic regularization, an experiment was conducted based on the predicted graphics of facade elements obtained from four pixel-wise annotated building facade datasets, Irregular Facades (IRFs), CMP Facade Database, ECP Paris, and ICG Graz50. The results demonstrate that the graphics regularized by our method align more closely with real facade elements in shape and edge. Moreover, our method avoids the prevalent issue of correctness degradation observed in existing methods. Compared with the predicted graphics, the average IoU and F1-score of our method-regularized graphics respectively increase by 0.001–0.017 and 0.000–0.012 across the datasets, while those of previous method-regularized graphics decrease by 0.002–0.021 and 0.002–0.015. The regularized graphics contribute to improving the precision and depth of semantic segmentation-based applications of building facades. They are also expected to be useful for the exploration of data mining on urban images in the future. Full article

Porcine rotavirus (PoRV) is one of the most devastating enteric pathogens causing gastroenteritis in pigs, particularly the sudden occurrence in recent years in China. To elucidate host–pathogen interactions and molecular mechanisms underlying PoRV pathogenesis, four-dimensional (4D) data-independent acquisition (DIA) proteomic (4D-DIA) analysis was performed to comprehensively quantify the differentially abundant proteins (DAPs) in PoRV-infected IPEC-J2 cells. A total of 8725 cellular proteins were identified with 279 more abundant and 356 down abundant proteins. A Western blot showed that the abundance of SA100A8, DAPK2, and FTL were in accordance with the acquired proteomic data using 4D-DIA analysis. Bioinformatics analyses of GO and KEGG demonstrated that various DAPs are involved in crucial biological processes and signaling pathways, such as immune response, signal transduction, metabolic pathways, autophagy, endoplasmic reticulum (ER) stress, and mitochondrial dysfunction. Notably, inflammatory features of host response upon PoRV infection were highlighted, with RT-qPCR confirming the significant upregulation of IL-1α, IL-6, IL-8, TNF-α, STAT1, and IRF9 transcript levels during infection. Altogether, our preliminary findings advance our understanding of PoRV pathogenesis and may shed light on identifying potential targets for the prevention and control of PoRV-associated gastroenteritis. Full article

Porcine reproductive and respiratory syndrome virus (PRRSV) remains one of the most important pathogens, resulting in huge economic losses to the global pig industry. Ipriflavone is an isoflavone derivative involved in various biological processes, showing anti-inflammatory, anti-apoptotic, antioxidant, and neuroprotective effects. However, the role of ipriflavone in antiviral immune response to PRRSV is unknown. In this study, we discovered that ipriflavone could significantly inhibit PRRSV replication. Moreover, ipriflavone inhibited PRRSV replication regardless of whether ipriflavone was added pre-, co-, or post-PRRSV infection, and ipriflavone mainly inhibited virus replication and assembly stages. Importantly, ipriflavone had the capacity to upregulate the expression levels of IFN-β and ISG56. Additionally, ipriflavone promoted the expression of RIG-I and MAVS, and induced phosphorylation of IRF3 and STAT1, while reducing PRRSV replication. Collectively, ipriflavone could enhance the RIG-I/IRF3 signaling pathway, thereby inhibiting PRRSV replication. These findings will provide an important theoretical basis for the development of therapeutic agents against PRRSV infection. Full article

Background/Objectives: Alcohol use disorder (AUD) is a major public health issue with rising global occurrence and metabolic consequences. Modeling the addictive behaviors associated with AUD remains inadequate and elusive. Even more so, models that are representative of AUD in concert with excessive caloric intake are limited. Some consequences of chronic alcohol use overlap with the metabolic phenotype of hypercaloric diets. Recently characterized metabolic dysfunction-associated steatotic liver disease with increased alcohol intake (MetALD) helps to differentiate these conditions. This study aims to investigate metabolic phenotypes and gene expression alterations in MetALD mice that are grouped by alcohol preference based on blood phosphatidylethanol levels and alcohol consumption. Methods: Mice were fed high-fat and chow diets, with water and 10% EtOH, for 13 weeks. mRNA sequencing was performed across multiple tissues including brain, liver, skeletal muscle, ileum, and white adipose tissue, and gut microbiome diversity was evaluated via 16S sequencing. Results: Key findings included reduced glucagon in alcohol-preferring mice with no significant differences in dyslipidemia and hepatic steatosis. Additionally, we observed reduced gut microbiome diversity and Wnt signaling with elevated acute-phase response genes in ileum tissue. Reduced Wnt and Hippo signaling in the brain and liver, respectively, was also revealed. Other gene ontologies discovered included increased neural inflammation and adipose mitochondrial translation. Nek3, Ntf3, Cux1, and Irf6 expression changes were shared across at least three tissues and may be potential biomarkers of alcohol addiction. Conclusions: This novel model assists future intervention research in the characterization of MetALD and identifies potential biomarkers of alcohol preference. Full article

Power metal-oxide-semiconductor field-effect transistors (MOSFETs) provide numerous advantages and are widely utilized in various power circuits. The junction temperature plays a critical role in determining the reliability, performance, and operational lifetime of power MOSFETs. Therefore, accurate monitoring of the junction temperature of power MOSFETs is essential to ensure the safe operation of power circuit systems. In bridge or motor drive circuits, MOSFETs often operate in a freewheeling state via the body diode, where the freewheeling current is typically variable. The proposed method for junction temperature measurement utilizes the body diode and is designed to accommodate varying forward currents. It also accounts for the temperature-dependent ideality factor to improve measurement accuracy. By integrating the forward voltage and forward current of the body diode, this approach reduces the required sampling frequency. To validate the method’s effectiveness, three representative types of power MOSFETs, a Si MOSFET (IRF520), a SiC MOSFET (C2M0080120D), and an aerospace-grade radiation-hardened MOSFET (RSCS25045T1RH), were used to measure junction temperatures before and after irradiation. Following ideality factor correction, the maximum absolute error compared to reference measurements from thermocouples and a thermal imager remained within 2 K across the temperature range of 300 K to 420 K. Experimental results confirm the feasibility of the proposed method. Full article

Background: The cerebral compliance (or compensatory reserve) index, RAP, is a critical yet underutilized physiological marker in the management of moderate-to-severe traumatic brain injury (TBI). While RAP offers promise as a continuous bedside metric, its broader cerebral physiological context remains partly understood. This study aims to characterize the burden of impaired RAP in relation to other key components of cerebral physiology. Methods: Archived data from 379 moderate-to-severe TBI patients were analyzed using descriptive and threshold-based methods across three RAP states (impaired, intact/transitional, and exhausted). Agglomerative hierarchical clustering, principal component analysis, and kernel-based clustering were applied to explore multivariate covariance structures. Then, high-frequency temporal analyses, including vector autoregressive integrated moving average impulse response functions (VARIMA IRF), cross-correlation, and Granger causality, were performed to assess dynamic coupling between RAP and other physiological signals. Results: Impaired and exhausted RAP states were associated with elevated intracranial pressure (p = 0.021). Regarding AMP, impaired RAP was associated with elevated levels, while exhausted RAP was associated with reduced pulse amplitude (p = 3.94 × 10⁻⁹). These two RAP states were also associated with compromised autoregulation and diminished perfusion. Clustering analyses consistently grouped RAP with its constituent signals (ICP and AMP), followed by brain oxygenation parameters (brain tissue oxygenation (PbtO₂) and regional cerebral oxygen saturation (rSO₂)). Cerebral autoregulation (CA) indices clustered more closely with RAP under impaired autoregulatory states. Temporal analyses revealed that RAP exhibited comparatively stronger responses to ICP and arterial blood pressure (ABP) at 1-min resolution. Moreover, when comparing ICP-derived and near-infrared spectroscopy (NIRS)-derived CA indices, they clustered more closely to RAP, and RAP demonstrated greater sensitivity to changes in these ICP-derived CA indices in high-frequency temporal analyses. These trends remained consistent at lower temporal resolutions as well. Conclusion: RAP relationships with other parameters remain consistent and differ meaningfully across compliance states. Integrating RAP into patient trajectory modelling and developing predictive frameworks based on these findings across different RAP states can map the evolution of cerebral physiology over time. This approach may improve prognostication and guide individualized interventions in TBI management. Therefore, these findings support RAP’s potential as a valuable metric for bedside monitoring and its prospective role in guiding patient trajectory modeling and interventional studies in TBI. Full article

Lumpy skin disease (LSD) is an invasive infectious disease caused by the lumpy skin disease virus (LSDV), which is detrimental to the production of cattle. LSDV encodes about 156 proteins, most of whose functions are still unknown. In this study, we found that the ORF137 protein was identified as one of the strongest inhibitors of IFN-β and ISG expression, determining LSDV ORF137 as a negative regulator of interferon (IFN) β signaling. Further evidence suggests that ORF137 interacts with the signal transduction factor IRF3 and inhibits the activation of IFN-β signaling by reducing Phospho-IRF3 (p-IRF3). Further investigation indicated that overexpression of ORF137 in BMEC could significantly inhibit the transcription of IFN-β and ISGs, thereby promoting the replication of LSDV. More importantly, through homologous recombination, we deleted the ORF137 gene from the LSDV/FJ/CHA/2021 strain and constructed the recombinant strain LSDV-ΔORF137-EGFP. Compared with the parental strain, LSDV-ΔORF137-EGFP showed a weakened effect on inhibiting the transcription of IFN-β and ISGs and a reduced replication level in infected MDBK cells. In summary, ORF137 facilitates LSDV replication by targeting IRF3 to inhibit IFN-β signaling. Our findings reveal a new mechanism by which LSDV suppresses the host antiviral response, which may facilitate the development of attenuated live vaccines for LSDV. Full article

Skin cancer is the most common cancer worldwide. The incidence of skin cancer has been increasing worldwide. Nearly 75% of all skin cancers are basal cell carcinomas (BCC), cutaneous squamous cell carcinoma (cSCC) represents approximately 20%, and those remaining are melanomas (4%) or other rare tumors (1%). Given the high cure rates and the ability to histologically confirm tumor clearance, surgical therapy is the gold standard for the treatment of skin cancer. Conventional surgery is the most employed technique for the removal of non-melanoma skin cancer (NMSCs). Mohs Micrographic Surgery (MMS) is the most precise surgical method for the treatment of non-melanoma skin cancer, allowing for 100% margin evaluation, being the gold-standard method for surgical treatment of non-melanoma skin cancer. Whenever it is possible to obtain wide margins (4 to 6 mm), cure rates vary from 70% to 99%. Imiquimod, a synthetic imidazoquinolinone amine, is a topical immune response modifier approved by the U.S. Food and Drug Administration (FDA) for the treatment of external anogenital warts, actinic keratosis (AK), and superficial basal cell carcinoma (sBCC). The efficacy of imiquimod is primarily attributed to its ability to modulate both innate and adaptive immune responses, as well as its direct effects on cancer cells. Imiquimod exerts its immunomodulatory effects by activating Toll-like receptors 7 and 8 (TLR7/8) on various immune cells, including dendritic cells, macrophages, and natural killer (NK) cells. Upon binding to these receptors, imiquimod triggers the MyD88-dependent signaling pathway, leading to the activation of nuclear factor kappa B (NF-κB) and interferon regulatory factors (IRFs). This cascade leads to the production of pro-inflammatory cytokines, including interferon-alpha (IFN-α), tumor necrosis factor-alpha (TNF-α), interleukin-12 (IL-12), and interleukin-6 (IL-6). These cytokines enhance local inflammation, recruit additional immune cells to the tumor site, and stimulate antigen presentation, thereby promoting an anti-tumor immune response. Radiation therapy (RTh) may be employed as a primary treatment to BCC. It may also be employed as an adjuvant treatment to surgery for SCC and aggressive subtypes of BCC. RTh triggers both direct and indirect DNA damage on cancer cells and generates reactive oxygen species (ROS) within cells. ROS trigger oxidative damage to DNA, proteins, and lipids, exacerbating the cellular stress and contributing to tumor cell death. Recently, immunotherapy emerged as a revolutionary treatment for all stages of SCC. Cemiplimab is a human programmed cell death 1 (PD-1)-blocking antibody that triggers a response to over 50% of patients with locally advanced and metastatic SCC. A randomized clinical trial (RCT) published in 2022 revealed that cemiplimab was highly effective in the neoadjuvant treatment of large SCCs. The drug promoted a significant tumor size decrease, enabling organ-sparing operations and a much better cosmetic effect. A few months ago, a RCT of cemiplimab on adjuvant therapy for locally aggressive SCC was published. Interestingly, cemiplimab was administered to patients with local or regional cutaneous squamous cell carcinoma after surgical resection and postoperative radiotherapy, at high risk for recurrence owing to nodal features, revealed that cemiplimab led to much lower risks both of locoregional recurrence and distant recurrence. Full article

Background: Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is characterized by chronic inflammation affecting the gastrointestinal tract and extraintestinal organs. The etiology of IBD is multifactorial, involving genetic, immunological, and environmental factors. Over 200 genetic loci have been associated with the disease, indicating a significant genetic predisposition. Despite advances in understanding its genetic basis, clinical management remains challenging due to heterogeneity in disease presentation and variable treatment responses. Current therapies, such as 5-aminosalicylates and biologics, are not universally effective, underscoring the need for reliable biomarkers to predict therapeutic responses. Objective: This study investigates the potential role of interferon regulatory factor 5 (IRF5) in the pathogenesis of IBD, with a particular focus on UC. Methods: We conducted a systematic analysis of colon biopsies from 30 adult patients diagnosed with UC and from 8 non-IBD controls. Immunostaining was performed to assess IRF5 expression in colonic tissues using the primary IRF5 antibody (1:300, Abcam, ab181553). Statistical analyses evaluated the correlation between IRF5-positive cell counts, disease activity, and inflammatory markers such as calprotectin. Results: Our analysis revealed a significant increase in IRF5-positive macrophage-like cells in the inflamed mucosa of IBD patients compared to healthy controls. The number of IRF5-positive cells showed a positive correlation with disease activity and calprotectin levels, indicating that higher IRF5 expression is associated with increased inflammation. Conclusions: This study demonstrates a significant correlation between IRF5 expression and disease activity in UC, suggesting that IRF5 may play a crucial role in the inflammatory processes of the disease. The findings propose IRF5 as a novel biomarker for therapeutic intervention in IBD. Further research is needed to clarify the mechanisms by which IRF5 contributes to IBD pathogenesis and to explore the therapeutic potential of targeting this pathway in clinical settings. Full article

Type 2 diabetes mellitus (T2DM), characterized by insulin resistance and chronic hyperglycemia, markedly increases the incidence and mortality of cardiovascular disease (CVD). Emerging preclinical evidence identifies the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS–STING) pathway as a critical mediator of diabetic cardiovascular inflammation. Metabolic stressors in T2DM—hyperglycemia, lipotoxicity, and mitochondrial dysfunction—induce leakage of mitochondrial and microbial double-stranded DNA into the cytosol, where it engages cGAS and activates STING. Subsequent TBK1/IRF3 and NF-κB signaling drives low-grade inflammation across cardiomyocytes, endothelial cells, macrophages, and fibroblasts. Genetic deletion of cGAS or STING in high-fat-diet-fed diabetic mice reduces NLRP3 inflammasome-mediated pyroptosis, limits atherosclerotic lesion formation, and preserves cardiac contractile performance. Pharmacological inhibitors, including RU.521 (cGAS antagonist), C-176/H-151 (STING palmitoylation blockers), and the TBK1 inhibitor amlexanox, effectively lower pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and improve left ventricular ejection fraction in diabetic cardiomyopathy and ischemia–reperfusion injury models. Novel PROTAC degraders targeting cGAS/STING and natural products such as Astragaloside IV and Tanshinone IIA further support the pathway’s druggability. Collectively, these findings position the cGAS–STING axis as a central molecular nexus linking metabolic derangement to cardiovascular pathology in T2DM and underscore its inhibition or targeted degradation as a promising dual cardiometabolic therapeutic strategy. Full article

Background/Objectives: Wet age-related macular degeneration (AMD) is a progressive retinal disease characterized by macular neovascularization (MNV). Currently, the standard treatment for wet AMD is intravitreal anti-VEGF administration, which aims to control disease activity by suppressing neovascularization. In clinical practice, the decision to continue or discontinue treatment is largely based on the presence of fluid on optical coherence tomography (OCT) and changes in visual acuity. However, discrepancies between anatomic and functional responses can occur during these assessments. Methods: This article presents an artificial intelligence (AI)-based classification model developed to objectively assess the response to anti-VEGF treatment in patients with AMD at 3 months. This retrospective study included 120 patients (144 eyes) who received intravitreal bevacizumab treatment. After bevacizumab loading treatment, the presence of subretinal/intraretinal fluid (SRF/IRF) on OCT images and changes in visual acuity (logMAR) were evaluated. Patients were divided into three groups: Class 0, active disease (persistent SRF/IRF); Class 1, good response (no SRF/IRF and ≥0.1 logMAR improvement); and Class 2, limited response (no SRF/IRF but with <0.1 logMAR improvement). Pre-treatment and 3-month post-treatment OCT image pairs were used for training and testing the artificial intelligence model. Based on this grouping, classification was performed with a Siamese neural network (ResNet-18-based) model. Results: The model achieved 95.4% accuracy. The macro precision, macro recall, and macro F1 scores for the classes were 0.948, 0.949, and 0.948, respectively. Layer Class Activation Map (LayerCAM) heat maps and Shapley Additive Explanations (SHAP) overlays confirmed that the model focused on pathology-related regions. Conclusions: In conclusion, the model classifies post-loading response by predicting both anatomic disease activity and visual prognosis from OCT images. Full article

The aim of this study was to conduct a comparative analysis of the effects of native quinoa grain with a high saponin content and quinoa grain subjected to preliminary saponin removal with low saponin content on growth, meat quality, biochemical blood composition, and the expression of genes related to muscle growth, gut health, and nutrient transport in broiler chickens. The control group of chickens received a standard diet. The SAP group feed contained quinoa grain without saponin removal (saponin level—5.20%) at 3% of the “Starter” feed mass and 5% of the “Grower” and “Finisher” feeds, maintaining the same nutritional values as the control group. The SAP-FREE group feed contained quinoa grain that was pre-treated to remove saponins by washing with water for 60 min at a temperature of 50 °C (saponin level—0.24%) in the same amount as the SAP group. The research results indicated certain advantages of unprocessed quinoa grain in relation to saponin content. Specifically, in the SAP group, the broiler performance index was at the same level as the control, while the SAP-FREE group had a high mortality rate (10%), resulting in a performance index that was 23.82 units lower than the control. The use of quinoa grain with high saponin content promoted better development of thigh muscles by 9.6% compared to the control (p = 0.008) and increased yields of wing, neck, and back muscles by 2.9 abs.% (p = 0.007) compared to the use of purified quinoa grain. The fat yield decreased by 1.7 abs.% (p = 0.015) with saponin-free quinoa compared to the control and by 2% (p = 0.008) compared to the high saponin group, making this feeding system viable for producing dietary meat. Upon stopping the feeding of purified quinoa, chickens showed a 34.0% increase in AST activity (p = 0.019) and a 15.7% increase in creatinine levels (p = 0.008), likely indicating intensified protein metabolism upon cessation of the inhibiting factor of purified quinoa. Molecular genetic studies revealed a 1.6-fold increase in IGF1 gene expression (p = 0.014) in breast muscle and a 69.12-fold increase (p = 0.010) in AvBD9 in the cecum due to high-saponin quinoa grain, while purified quinoa increased GHR gene expression by 3.29 times (p = 0.039) in breast muscle and decreased IRF7 activity to 2^−ΔΔCT = 0.54 (p = 0.017). The expression of transporter protein genes decreased to low or undetectable levels, indicating the presence of anti-nutritional factors and the need for further research on feeding quinoa with the addition of proteases. Thus, high-saponin quinoa grain, unlike purified quinoa, positively influences gut health and bird survival, maintaining performance levels similar to the control, suggesting the feasibility of using unprocessed quinoa in poultry nutrition, thus avoiding additional costs in feed preparation. Full article

The global impact of COVID-19 was staggering, with millions of cases and related mortality reported worldwide. Genetic variations play a significant role in determining an individual’s susceptibility to SARS-CoV-2 infection and progress to severe disease. This pilot study provides an experimental approach using WES to identify certain rare and novel genetic variants that might affect an individual’s susceptibility to the risk of SARS-CoV-2 infection, offering an initial exploration of these genetic variants. In the study cohort with 16 patients, the mortality rate was higher in male patients due to severe disease. There was a substantial burden of comorbidity, including hypertension, ischemic heart disease, and T2DM, conditions which independently increase the risk of adverse outcomes in COVID-19 patients. A total of 4478 variants were identified, distributed across 322 genes within the cohort. The majority of these variants were missense substitutions along with frameshift variants, inframe insertions/deletions (indels), and nonsense variants. The variants were further categorized by types to include single-nucleotide polymorphisms (SNPs), deletions (DEL), and insertions (INS). The gene with the highest number of variants was HLA-DRB1, followed by HLA-B, ABO, HPS4, and SP110 displaying both common polymorphisms and rare variants. Moreover, the HLA-B gene exhibited the highest number of rare candidate variants, followed by AK2, IRF7, KMT2D, TAP1, and HLA-DRB1. Several genes harbored multiple novel variants, including TAP1, AK2, G6PC3, HLA-B, IL12RB2, and ITGB2. The frequencies of the identified variants were found to be either zero or extremely low (below 1% threshold) in the Middle Eastern or in the overall combined population, suggesting that these are indeed rare and do not represent common indigenous polymorphisms. Functional enrichment analysis of the constructed protein–protein interaction network in our preliminary findings revealed that the identified genes are primarily enriched in pathways associated with immune deficiency and DNA repair. This initial exploration of genetic variants in COVID-19 susceptibility provides a foundation for future large-scale studies. Full article

Amid the health-conscious consumption trend, functional foods rich in γ-aminobutyric acid (GABA) and vitamin B9 are gaining prominence. Foxtail millet, a traditional grain naturally abundant in these nutrients, faces quality assessment challenges due to the time-consuming and destructive nature of conventional methods, hindering large-scale screening. This study pioneers the systematic application of hyperspectral imaging (HSI) for nondestructive detection of GABA and vitamin B9 in millet. Utilizing spectral data from 190 samples across 19 varieties, we developed an innovative “coarse-fine” feature wavelength selection strategy. First, interval-based algorithms (iRF, iVISSA) screened highly correlated wavelength subsets. Second, model population analysis (MPA) algorithms (CARS, BOSS) identified optimal core wavelengths, boosting model efficiency and robustness. Based on this, a stacked BiLSTM–Adaboost model was built, integrating bidirectional long short-term memory networks for sequence dependency and adaptive boosting for enhanced generalization. This enables efficient, rapid, nondestructive, and precise nutrient detection. This interdisciplinary breakthrough establishes a novel pathway for millet nutritional assessment, deepens fundamental research, and provides core support for industrial upgrading, breeding, quality control, and functional food development, supporting national health. Full article

Background: The function and mechanism of N6-methyladenosine (m6A) methylation in pressure-overload cardiac fibrosis remains limited and unclear. This study aims to analyze and predict m6A modifications present in mouse hearts because of transverse aortic constriction (TAC). Materials and Methods: Twelve male C57BL/6 mice were randomly assigned to two groups, TAC group and sham group. The RNA Dot Blot assay was employed to evaluate the overall m6A methylation levels in both TAC and sham mice. The expression level of m6A-related enzymes were investigated through RT-PCR and Western blotting. MeRIP-seq and RNA-seq analyses were conducted to identify differentially modified m6A genes and mRNA expression genes. The protein–protein interaction (PPI) network was carried out to choose potential hub genes. Additionally, the transcription factor (TF)–microRNA (miRNA) coregulatory network and the drug–hub gene interaction network were built based on these hub genes. Furthermore, molecular docking simulations were also performed to analyze the interactions between drugs and hub genes. Results: Compared with the sham group, the TAC group demonstrated elevated levels of global m6A methylation. METTL3 and METTL14 were significantly upregulated, whereas FTO and ALKBH5 were significantly downregulated following TAC. MeRIP-seq analysis identified 17,806 m6A peaks associated with 9184 genes and 16,392 m6A peaks associated with 8550 genes in the TAC and sham groups, respectively. In conjunction with RNA-seq data, 66 genes were identified as exhibiting concurrent differences in both m6A methylation levels and mRNA expression. Six hub genes, Cd33, Irf4, Nr4a2, Hspa1b, Nr4a1, and Adcy1, were identified through the construction of a PPI network. The TF-miRNA coregulatory network contains six hub genes, 31 miRNAs, and 24 TFs. The drug–hub genes interaction network included five hub genes and 36 candidate drugs. Conclusions: The m6A modification is prevalent in TAC-induced cardiac fibrosis and significantly contributes to the fibrotic process by regulating critical genes. In the future, it may emerge as one of the potential cardiac fibrosis therapeutic targets. Full article