High-resolution maps show that rubber causes substantial deforestation.

Understanding the effects of cash crop expansion on natural forest is of fundamental importance. However, for most crops there are no remotely sensed global maps1, and global deforestation impacts are estimated using models and extrapolations. Natural rubber is an example of a principal commodity for which deforestation impacts have been highly uncertain, with estimates differing more than fivefold1-4. Here we harnessed Earth observation satellite data and cloud computing5 to produce high-resolution maps of rubber (10 m pixel size) and associated deforestation (30 m pixel size) for Southeast Asia. Our maps indicate that rubber-related forest loss has been substantially underestimated in policy, by the public and in recent reports6-8. Our direct remotely sensed observations show that deforestation for rubber is at least twofold to threefold higher than suggested by figures now widely used for setting policy4. With more than 4 million hectares of forest loss for rubber since 1993 (at least 2 million hectares since 2000) and more than 1 million hectares of rubber plantations established in Key Biodiversity Areas, the effects of rubber on biodiversity and ecosystem services in Southeast Asia could be extensive. Thus, rubber deserves more attention in domestic policy, within trade agreements and in incoming due-diligence legislation.

Berberine increases the killing effect of pirarubicin on HCC cells by inhibiting ATG4B-autophagy pathway.

Pirarubicin (THP) is a new generation of cell cycle non-specific anthracycline-based anticancer drug. In the clinic, THP and THP combination therapies have been shown to be effective in hepatocellular carcinoma (HCC) patients with transcatheter arterial chemoembolization (TACE) without serious side effects. However, drug resistance limits its therapeutic efficacy. Berberine (BBR), an isoquinoline alkaloid, has been shown to possess antitumour properties against various malignancies. However, the synergistic effect of BBR and THP in the treatment of HCC is unknown. In the present study, we demonstrated for the first time that BBR sensitized HCC cells to THP, including enhancing THP-induced growth inhibition and apoptosis of HCC cells. Moreover, we found that BBR sensitized THP by reducing the expression of autophagy-related 4B (ATG4B). Mechanistically, the inhibition of HIF1α-mediated ATG4B transcription by BBR ultimately led to attenuation of THP-induced cytoprotective autophagy, accompanied by enhanced growth inhibition and apoptosis in THP-treated HCC cells. Tumor-bearing experiments in nude mice showed that the combination treatment with BBR and THP significantly suppressed the growth of HCC xenografts. These results reveal that BBR is able to strengthen the killing effect of THP on HCC cells by repressing the ATG4B-autophagy pathway, which may provide novel insights into the improvement of chemotherapeutic efficacy of THP, and may be conducive to the further clinical application of THP in HCC treatment.

RNAincoder: a deep learning-based encoder for RNA and RNA-associated interaction.

Ribonucleic acids (RNAs) involve in various physiological/pathological processes by interacting with proteins, compounds, and other RNAs. A variety of powerful computational methods have been developed to predict such valuable interactions. However, all these methods rely heavily on the 'digitalization' (also known as 'encoding') of RNA-associated interacting pairs into a computer-recognizable descriptor. In other words, it is urgently needed to have a powerful tool that can not only represent each interacting partner but also integrate both partners into a computer-recognizable interaction. Herein, RNAincoder (deep learning-based encoder for RNA-associated interactions) was therefore proposed to (a) provide a comprehensive collection of RNA encoding features, (b) realize the representation of any RNA-associated interaction based on a well-established deep learning-based embedding strategy and (c) enable large-scale scanning of all possible feature combinations to identify the one of optimal performance in RNA-associated interaction prediction. The effectiveness of RNAincoder was extensively validated by case studies on benchmark datasets. All in all, RNAincoder is distinguished for its capability in providing a more accurate representation of RNA-associated interactions, which makes it an indispensable complement to other available tools. RNAincoder can be accessed at https://idrblab.org/rnaincoder/.

A task-specific encoding algorithm for RNAs and RNA-associated interactions based on convolutional autoencoder.

RNAs play essential roles in diverse physiological and pathological processes by interacting with other molecules (RNA/protein/compound), and various computational methods are available for identifying these interactions. However, the encoding features provided by existing methods are limited and the existing tools does not offer an effective way to integrate the interacting partners. In this study, a task-specific encoding algorithm for RNAs and RNA-associated interactions was therefore developed. This new algorithm was unique in (a) realizing comprehensive RNA feature encoding by introducing a great many of novel features and (b) enabling task-specific integration of interacting partners using convolutional autoencoder-directed feature embedding. Compared with existing methods/tools, this novel algorithm demonstrated superior performances in diverse benchmark testing studies. This algorithm together with its source code could be readily accessed by all user at: https://idrblab.org/corain/ and https://github.com/idrblab/corain/.

Strategy for Identifying a Robust Metabolomic Signature Reveals the Altered Lipid Metabolism in Pituitary Adenoma.

Despite the well-established connection between systematic metabolic abnormalities and the pathophysiology of pituitary adenoma (PA), current metabolomic studies have reported an extremely limited number of metabolites associated with PA. Moreover, there was very little consistency in the identified metabolite signatures, resulting in a lack of robust metabolic biomarkers for the diagnosis and treatment of PA. Herein, we performed a global untargeted plasma metabolomic profiling on PA and identified a highly robust metabolomic signature based on a strategy. Specifically, this strategy is unique in (1) integrating repeated random sampling and a consensus evaluation-based feature selection algorithm and (2) evaluating the consistency of metabolomic signatures among different sample groups. This strategy demonstrated superior robustness and stronger discriminative ability compared with that of other feature selection methods including Student's t-test, partial least-squares-discriminant analysis, support vector machine recursive feature elimination, and random forest recursive feature elimination. More importantly, a highly robust metabolomic signature comprising 45 PA-specific differential metabolites was identified. Moreover, metabolite set enrichment analysis of these potential metabolic biomarkers revealed altered lipid metabolism in PA. In conclusion, our findings contribute to a better understanding of the metabolic changes in PA and may have implications for the development of diagnostic and therapeutic approaches targeting lipid metabolism in PA. We believe that the proposed strategy serves as a valuable tool for screening robust, discriminating metabolic features in the field of metabolomics.

Hydrolysis mechanism of the cyclohexaborate anion: Unraveling the intricacies.

B 6 O 7 OH 6 2 - is a highly polymerized borate anion of three six-membered rings. Limited research on the B 6 O 7 OH 6 2 - hydrolysis mechanism under neutral solution conditions exists. Calculations based on density functional theory show that B 6 O 7 OH 6 2 - undergoes five steps of hydrolysis to form H3BO3 and B OH 4 - . At the same time, there are a small number of borate ions with different degrees of polymerization during the hydrolysis process, such as triborate, tetraborate, and pentaborate anions. The structure of the borate anion and the coordination environment of the bridging oxygen atoms control the hydrolysis process. Finally, this work explains that in existing experimental studies, the reason for the low B 6 O 7 OH 6 2 - content in solution environments with low total boron concentrations is that it depolymerizes into other types of borate ions and clarifies the borate species. The conversion relationship provides a basis for identifying the possibility of various borate ions existing in the solution. This work also provides a certain degree of theoretical support for the cause of the "dilution to salt" phenomenon.

Induced Ferroptosis Pathway by Regulating Cellular Lipid Peroxidation With Peroxynitrite Generator for Reversing "Cold" Tumors.

Overcoming the resistance of tumor cells to apoptosis and immunosuppression is an important challenge to improve tumor immunotherapy. Non-apoptotic death mode of ferroptosis has been regarded as a new strategy to enhance tumor immunotherapy against drug-resistant cancers. The lethal accumulation of lipid peroxides (LPO) determines the progress of ferroptosis. The high susceptibleness of ferroptosis provides an opportunity for combating triple-negative breast cancer. Reactive nitrogen species (RNS) produced by nitric oxide (NO) and reactive oxygen species (ROS) is more lethal than ROS for tumor cells. Herein, an RNS-mediated immunotherapy strategy for inducing ferroptosis pathway is proposed by improving LPO accumulation, and constructed a multifunctional liposome (Lipo-MT-SNAP) comprised of peroxynitrite (ONOO-) generator, tumor targeted group, inhibiting glutathione peroxidase 4 (GPX4), and basic units (dipalmitoyl phosphatidylcholine and cholesterol). The significant enhancement of LPO resulted from the intense oxidative damage of ONOO- impaired synthesis of GPX4 by depleting glutathione, which further amplified ferroptosis and triggered immunogenic cell death. In vivo, RNS-mediated photoimmunotherapy can promote polarization of M2 to M1 macrophages and dendritic cells maturation, further infiltrate T cells, regulate the secretion of inflammatory factors, and reprogram the tumor microenvironment. The powerful RNS-mediated ferroptosis induces strong immunogenicity and effectively inhibit tumor proliferation.

ncRNAInter: a novel strategy based on graph neural network to discover interactions between lncRNA and miRNA.

In recent years, many studies have illustrated the significant role that non-coding RNA (ncRNA) plays in biological activities, in which lncRNA, miRNA and especially their interactions have been proved to affect many biological processes. Some in silico methods have been proposed and applied to identify novel lncRNA-miRNA interactions (LMIs), but there are still imperfections in their RNA representation and information extraction approaches, which imply there is still room for further improving their performances. Meanwhile, only a few of them are accessible at present, which limits their practical applications. The construction of a new tool for LMI prediction is thus imperative for the better understanding of their relevant biological mechanisms. This study proposed a novel method, ncRNAInter, for LMI prediction. A comprehensive strategy for RNA representation and an optimized deep learning algorithm of graph neural network were utilized in this study. ncRNAInter was robust and showed better performance of 26.7% higher Matthews correlation coefficient than existing reputable methods for human LMI prediction. In addition, ncRNAInter proved its universal applicability in dealing with LMIs from various species and successfully identified novel LMIs associated with various diseases, which further verified its effectiveness and usability. All source code and datasets are freely available at https://github.com/idrblab/ncRNAInter.

Biological activities of drug inactive ingredients.

In a drug formulation (DFM), the major components by mass are not Active Pharmaceutical Ingredient (API) but rather Drug Inactive Ingredients (DIGs). DIGs can reach much higher concentrations than that achieved by API, which raises great concerns about their clinical toxicities. Therefore, the biological activities of DIG on physiologically relevant target are widely demanded by both clinical investigation and pharmaceutical industry. However, such activity data are not available in any existing pharmaceutical knowledge base, and their potentials in predicting the DIG-target interaction have not been evaluated yet. In this study, the comprehensive assessment and analysis on the biological activities of DIGs were therefore conducted. First, the largest number of DIGs and DFMs were systematically curated and confirmed based on all drugs approved by US Food and Drug Administration. Second, comprehensive activities for both DIGs and DFMs were provided for the first time to pharmaceutical community. Third, the biological targets of each DIG and formulation were fully referenced to available databases that described their pharmaceutical/biological characteristics. Finally, a variety of popular artificial intelligence techniques were used to assess the predictive potential of DIGs' activity data, which was the first evaluation on the possibility to predict DIG's activity. As the activities of DIGs are critical for current pharmaceutical studies, this work is expected to have significant implications for the future practice of drug discovery and precision medicine.

Mid-infrared tunable absorber based on an Ag/SiO2/VO2/Ag/VO2 multilayer structure and its molecular sensing capability.

We present a design of middle-infrared modulation absorbers based on vanadium dioxide (VO2). By using the electron beam evaporation technique, the Ag/SiO2/VO2/Ag/VO2 multilayer structure can achieve double band strong absorption in the mid-infrared, and dynamically adjust the absorption performance through VO2. The simulation results demonstrate a remarkable absorption rate of 91.8% and 98.9% at 9.09 µm and 10.25 µm, respectively. The high absorption is elucidated by analyzing the field strength distribution in each layer. Meanwhile, based on the phase change characteristics of VO2, the absorber has exceptional thermal regulation, with a remarkable 78% heat regulation range in the mid-infrared band. The size altering of the absorbing layer is effective in enhancing and optimizing the structure's absorption performance. The structure is used to characterize probe molecules of CV and R6 G by mid-infrared spectroscopy, which illustrates an impressive limit of detection (LOD) of 10-7 M for both substances. These results provide valuable insights for designing future high-performance tunable optical devices.

Activation of Notch1-GATA3 pathway in asthma bronchial epithelial cells induced by acute PM2.5 exposure and the potential protective role of microRNA-139-5p.

OBJECTIVE: PM2.5 is closed linked to asthma exacerbation. The Notch1 pathway acts as an important pathway, ultimately inducing T-helper cells that express GATA3 and its corresponding Th2 cytokines. The regulatory effects of miR-139-5p on the Notch1 pathway have been indicated in cancer. However, studies on miR-139-5p have not applied asthma-related models. The role of miR-139-5p and its regulatory effects on the Notch1-GATA3 pathway in asthma exacerbation induced by acute PM2.5 exposure has not been elucidated. We hypothesize that acute PM2.5 exposure induces asthma exacerbation by regulating the expression of miR-139-5p and activating the Notch1-GATA3 pathway. METHODS: We first employed Diseased Human Bronchial Epithelial Cells-Asthma cells to establish an in vitro model of acute exposure to PM2.5, and explored the relationship between the different concentrations and durations of acute PM2.5 exposure and the activation of Notch1-GATA3 pathway. We investigated the protein and mRNA expression changes of Notch1, upstream Jagged1, downstream GATA3, as well as the regulatory effect of miR-139-5p involved in it. RESULTS: The miR-139-5p expression increased within 24 h of PM2.5 exposure. However, if PM2.5 exposure was sustained, miR-139-5p expression turned to decrease, accompanied by upregulations of the mRNA and protein expression of Notch1-GATA3 pathway. Overexpression of miR-139-5p blocked Notch1-GATA3 pathway activation induced by acute PM2.5 exposure. CONCLUSION: Acute PM2.5 exposure can activate Notch1-GATA3 pathway in asthma bronchial epithelial cells model, which might be involved in PM2.5-induced asthma exacerbation. miR-139-5p has a potential protective role of inhibiting PM2.5-induced asthma airway inflammation by targeting Notch1.

MiR26a reverses enzalutamide resistance in a bone-tumor targeted system with an enhanced effect on bone metastatic CRPC.

Resistance to androgen receptor (AR) inhibitors, including enzalutamide (Enz), as well as bone metastasis, are major challenges for castration-resistant prostate cancer (CRPC) treatment. In this study, we identified that miR26a can restore Enz sensitivity and inhibit bone metastatic CRPC. To achieve the highest combination effect of miR26a and Enz, we developed a cancer-targeted nano-system (Bm@PT/Enz-miR26a) using bone marrow mesenchymal stem cell (BMSC) membrane and T140 peptide to co-deliver Enz and miR26a. The in vitro/in vivo results demonstrated that miR26a can reverse Enz resistance and synergistically shrink tumor growth, invasion, and metastasis (especially secondary metastasis) in both subcutaneous and bone metastatic CRPC mouse models. We also found that the EZH2/SFRP1/WNT5A axis may be involved in this role. These findings open new avenues for treating bone metastatic and Enz-resistant CRPC.

Retracted: LOC101060264 Silencing Suppresses Invasion and Metastasis of Human Colon Cancer.

The Editors of Medical Science Monitor wish to inform you that the above manuscript has been retracted from publication due to concerns with the credibility and originality of the study, the manuscript content, and the Figure images.Reference:Weihua Yu, Yunxia Wang, Lan Liu, Shuai Li, Kongxi Zhu. LOC101060264 Silencing Suppresses Invasion and Metastasis of Human Colon Cancer. Med Sci Monit, 2020; 26: e920270. DOI: 10.12659/MSM.920270.

Circular RNA Pum_0014 Targets miR-146a-5p/NF2 Axis to Regulate VEGF/PAK1 Pathway and Reduce H2O2-induced Cardiomyocyte Apoptosis.

Circular RNAs (circRNAs) have emerged as essential regulators in cardiovascular disease, including acute myocardial infarction (AMI). This study investigated the role of circRNA Pum1_0014 in myocardial infarction (MI) and its underlying mechanisms using an H9C2 cell model. Through Sanger sequencing, nucleic acid electrophoresis, RNase R, and transcriptional inhibition experiments, Pum1_0014 was identified as a novel circRNA. The cell localization of circRNA Pum1_0014 was detected by qPCR and fluorescence in situ hybridization, and the results revealed that circRNA Pum1_0014 is predominantly located in the cytoplasm. StarBase (URL: http://starbase.sysu.edu.cn/) and TargetScan (URL: https://www.targetscan.org/vert_80/) were used to predict circRNA Pum1_0014 targeting miRNAs and miRNA targeting mRNA, and the results identified miR-146a-5p as a potential target of Pum1_0014, which in turn targets NF2. The plasmid encoding the mutant circRNA Pum1_0014 or the 3'UTR mutant NF2 was constructed, and the interaction between Pum1_0014 and miR-146a-5p or miR-146a-5p and NF2 was detected by luciferase reporter gene assay. The results confirmed the interactions between Pum1_0014, miR-146a-5p, and NF2. In the MI cell model, upregulation of circRNA Pum1_0014 and NF2 and downregulation of miR-146a-5p were observed. Knockdown of circRNA Pum1_0014 inhibited NF2 expression and activated the VEGF/PAK1 pathway, reducing cardiomyocyte apoptosis. Conversely, inhibition of miR-146a-5p and overexpression of NF2 had opposite effects. These findings suggest that circRNA Pum1_0014 acts through the miR-146a-5p/NF2 axis to reduce cardiomyocyte apoptosis in MI via the VEGF/PAK1/NF2 pathway.

Light-Triggered Reversible Tuning of Second-Harmonic Generation in a Photoactive Plasmonic Molecular Nanocavity.

The ultrasmall mode volume and ultralarge local field enhancement of compact plasmonic nanocavities have been widely explored to amplify a variety of optical phenomena at the nanoscale. Other than passively generating near-field enhancements, dynamic tuning of their intensity and associated nonlinear optical processes such as second-harmonic generation (SHG) play vital roles in the field of active nanophotonics. Here we apply a host-guest molecular complex to construct a photoswitchable molecule-sandwiched metallic particle-on-film nanocavity (MPoFN) and demonstrate both light-controlled linear and nonlinear optical tuning. Under alternating illumination of ultraviolet (UV) and visible light, the photoactive plasmonic molecular nanocavity shows reversible switching of both surface-enhanced Raman scattering (SERS) and plasmon resonance. Surprisingly, we observe more significant modulation of SHG from this photoactive MPoFN, which can be explained qualitatively by the quantum conductivity theory (QCT). Our study could pave the way for developing miniaturized integrated optical circuits for ultrafast all-optical information processing and communication.

Sirtuin 2 Exerts Regulatory Functions on Radiation-Induced Myocardial Fibrosis in Mice by Mediating H3K27 Acetylation of Galectin-3 Promoter.

Background: Sirtuin 2 (SIRT2) and galectin-3 have been shown to protect the heart against fibrosis. However, their impacts on radiation-induced myocardial fibrosis (RIMF) remain to be elucidated. To deepen this understanding, the current study sought to explore the effects of SIRT2 and galectin-3 on RIMF and the underlying mechanisms. Methods: Galectin-3 knockout mice were obtained, and a radiation-induced heart damage (RIHD) mouse model was induced by local radiation exposure to the heart. Lentivirus transfection was then performed, and heart function, fibrosis of heart tissues, and levels of SIRT2, galectin-3, and fibrosis-related markers collagen type-I/-III and matrix metalloproteinase (MMP)2/MMP9 were respectively assessed by echocardiography, hematoxylin-eosin and Masson staining, reverse transcription-quantitative polymerase chain reaction, Western blot, and immunofluorescence staining. Additionally, Western blot and chromatin immunoprecipitation were used to test H3K27 acetylation levels and the binding of H3K27ac to galectin-3, respectively. Results: After radiation exposure, heart tissues from the galectin-3 knockout mice had a smaller fibrotic area compared to normal mice, with reduced expression levels of collagen type-I/-III and MMP2/MMP9. SIRT2 was down-regulated and galectin-3 was up-regulated after RIHD treatment. The histone deacetylase inhibitor sirtinol promoted galectin-3 expression and H3K27 acetylation in a time-dependent manner, and increased H3K27ac enrichment in the galectin-3 promoter. Overexpression of SIRT2 down-regulated H3K27ac, collagen type-I/-III, and MMP2/MMP9 expression levels, and reduced the fibrotic area in mouse heart tissues. However, these effects were reversed by the additional overexpression of galectin-3. Conclusions: SIRT2 facilitates deacetylation of H3K27 to inhibit galectin-3 transcription, thus ameliorating RIMF in mice.

Divergent Synthesis of 17-nor-Cephalotane Diterpenoids through Developed Ynol-diene Cyclization.

On the basis of a novel ynol-diene cyclization developed as a rapid access to tropone unit, the first divergent strategy to 17-nor-cephalotane diterpenoids has been successfully established. Combining with a bioinspired stereoselective dual hydrogenation, the divergent total synthesis of (+)-3-deoxyfortalpinoid F, (+)-harringtonolide, (-)-fortalpinoids M/N/P, and analog (-)-20-deoxocephinoid P have been achieved in 14-17 linear longest steps starting from commercially available materials.

Ultrathin In2 O3 Nanosheets toward High Responsivity and Rejection Ratio Visible-Blind UV Photodetection.

Photoelectrochemical-type visible-blind ultraviolet photodetectors (PEC VBUV PDs) have gained ever-growing attention due to their simple fabrication processes, uncomplicated packaging technology, and high sensitivity. However, it is still challenging to achieve high-performance PEC VBUV PDs based on a single material with good spectral selectivity. Here, it is demonstrated that individual ultrathin indium oxide (In2 O3 ) nanosheets (NSs) are suitable for designing high-performance PEC VBUV PDs with high responsivity and UV/visible rejection ratio for the first time. In2 O3 NSs PEC PDs show excellent UV photodetection capability with an ultrahigh photoresponsivity of 172.36 mA W-1 and a high specific detectivity of 4.43 × 1011 Jones under 254 nm irradiation, which originates from the smaller charge transfer resistance (Rct ) at the In2 O3 NSs/electrolyte interface. The light absorption of In2 O3 NSs takes a blueshift due to the quantum confinement effect, granting good spectral selectivity for visible-blind detection. The UV/visible rejection ratio of In2 O3 NSs PEC PDs is 1567, which is 30 times higher than that of In2 O3 nanoparticles (NPs) and exceeds all recently reported PEC VBUV PDs. Moreover, In2 O3 NSs PEC PDs show good stability and good underwater imaging capability. The results verify that ultrathin In2 O3 NSs have potential in underwater optoelectronic devices.

MetaFS: Performance assessment of biomarker discovery in metaproteomics.

Metaproteomics suffers from the issues of dimensionality and sparsity. Data reduction methods can maximally identify the relevant subset of significant differential features and reduce data redundancy. Feature selection (FS) methods were applied to obtain the significant differential subset. So far, a variety of feature selection methods have been developed for metaproteomic study. However, due to FS's performance depended heavily on the data characteristics of a given research, the well-suitable feature selection method must be carefully selected to obtain the reproducible differential proteins. Moreover, it is critical to evaluate the performance of each FS method according to comprehensive criteria, because the single criterion is not sufficient to reflect the overall performance of the FS method. Therefore, we developed an online tool named MetaFS, which provided 13 types of FS methods and conducted the comprehensive evaluation on the complex FS methods using four widely accepted and independent criteria. Furthermore, the function and reliability of MetaFS were systematically tested and validated via two case studies. In sum, MetaFS could be a distinguished tool for discovering the overall well-performed FS method for selecting the potential biomarkers in microbiome studies. The online tool is freely available at https://idrblab.org/metafs/.

Bioinformatics analysis of potential common pathogenic mechanisms for systemic lupus erythematosus and acute myocardial infarction.

BACKGROUND: Systemic lupus erythematosus (SLE) patients have a higher risk of acute myocardial infarction (AMI) compared to the general population. However, the underlying common mechanism of this association is not fully understood. This study aims to investigate the molecular mechanism of this complication. METHODS: Gene expression profiles of SLE (GSE50772) and AMI (GSE66360) were obtained from the Gene Expression Omnibus (GEO) database. Common differentially expressed genes (DEGs) in SLE and AMI were identified, and functional annotation, protein-protein interaction (PPI) network analysis, module construction, and hub gene identification were performed. Additionally, transcription factor (TF)-gene regulatory network and TF-miRNA regulatory network were constructed for the hub genes. RESULTS: 70 common DEGs (7 downregulated genes and 63 upregulated genes) were identified and were mostly enriched in signaling pathways such as the IL-17 signaling pathway, TNF signaling pathway, lipid metabolism, and atherosclerosis. Using cytoHubba, 12 significant hub genes were identified, including IL1B, TNF, FOS, CXCL8, JUN, PTGS2, FN1, EGR1, CXCL1, DUSP1, MMP9, and ZFP36. CONCLUSIONS: This study reveals a common pathogenesis of SLE and AMI and provides new perspectives for further mechanism research. The identified common pathways and hub genes may have important clinical implications for the prevention and treatment of AMI in SLE patients.