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Hua Wang

Publications and source records attributed to Hua Wang.

At least 19 recordsLinked to original sources
PubMed2026

MicroRNA-181a-5p promotes papillary thyroid carcinoma progress via the PTEN/AKT pathway.

The objective of this investigation was to determine the expression profile and latent mechanism of microRNA-181a-5p (miR-181a-5p) in the genesis and progression of papillary thyroid cancer (PTC). MiR-181a-5p was discovered to be upregulated in PTC tissues and cells in this study, as confirmed by RT‒qPCR and The Cancer Genome Atlas database. Notably, in PTC patients, the miR-181a-5p level was linked to tumor size and thyroid capsule invasion. A series of experiments demonstrated that miR-181a-5p upregulation in PTC cells notably enhanced proliferation, motility, and invasion, whereas suppressing miR-181a-5p hindered these functions. Western blotting revealed that miR-181a-5p suppressed PTEN expression, boosting the activation of phosphorylated AKT (P-AKT). According to predictive bioinformatics research and luciferase reporter gene tests, miR-181a-5p may target a specific binding site on the PTEN 3'UTR. To sum up, this study indicated that miR-181a-5p promoted PTC progression through the PTEN/Akt pathway. This investigation reveals a potential mechanism for PTC progression and provides a foundation for clinical therapies.

MicroRNAs↗
PubMed2026

Association between packed red blood cell transfusion and clinical deterioration in neonatal necrotizing enterocolitis: a systematic review and meta-analysis.

BACKGROUND: No systematic review has evaluated the existing evidence regarding the association between packed red blood cell (pRBC) transfusion and clinical worsening of necrotizing enterocolitis (NEC) in neonates. This systematic review and meta-analysis was conducted to address this knowledge gap. MATERIALS AND METHODS: We searched the Cochrane Library, EBSCO, Embase, Web of Science, Google Scholar, and PubMed for studies on pRBC transfusion and NEC published before May 10, 2025. Relevant articles were selected through title, abstract, and full-text screening. English-language case-control studies or cohort studies, or randomized controlled trials involving newborns with NEC that compared pRBC transfusion with no transfusion and reported changes in NEC clinical status were included. Review articles, systematic reviews, case reports, editorials, animal studies, duplicate publications, and studies with incomplete data were excluded. RESULTS: Five studies involving 971 neonates with NEC were included. The pooled analysis demonstrated a potential association between pRBC transfusion and clinical deterioration of NEC in neonates (odds ratio: 6.05, 95% confidence interval: 3.02-12.14). CONCLUSIONS: pRBC transfusion was associated with an exacerbation of NEC in neonates. However, these findings should be interpreted cautiously because of the small number of eligible studies included in this meta-analysis, and future large-scale, well-designed studies are needed to confirm the observed association.

Humans↗
PubMed2026

ELN orchestrates prometastatic and immunosuppressive niche in bladder cancer via TGFB1 autocrine signaling.

Bladder cancer (BCa) mortality is mainly driven by metastatic dissemination and an immunosuppressive tumor microenvironment. Here, we identify ELN (tropoelastin), an extracellular matrix protein abundantly secreted by cancer-associated fibroblasts (CAFs), as a critical determinant of these processes and a marker of poor prognosis. ELN promotes epithelial-mesenchymal transition (EMT), facilitates lymphatic spread, and induces immune dysfunction characterized by macrophage polarization toward an M2 phenotype and T cell exhaustion. Mechanistically, ELN functions as a binding partner of TGF-β receptor 2 (TGFBR2), thereby triggering SMAD2/3-dependent TGF-β1 secretion and establishing a feed forward signaling loop. This ELN/TGFBR2/TGF-β1 axis amplifies metastatic capacity and immunosuppressive signaling, ultimately accelerating disease progression and diminishing responsiveness to immune checkpoint blockade. Functional studies in BCa organoids and murine models demonstrated that pharmacologic blockade of the ELN-TGFBR2 interaction effectively suppressed tumor metastasis and restored antitumor immunity. Collectively, our findings establish ELN as a CAF-derived driver of metastasis and immune evasion in BCa. Targeting the ELN-TGFBR2 interaction offers a promising therapeutic strategy to limit metastatic progression and enhance the efficacy of immunotherapy in this lethal disease.

Animals↗
PubMed2025

Tannin-bearing hydrogel adhesives with enhanced mechanical and adhesion strength in response to protein leakage.

Anastomotic leaks are among the most severe side effects following abdominal surgeries. Conventional surgical sealants and emerging hydrogel adhesives often lose mechanical and adhesion strength when exposed to leaked digestive enzymes. Here, we report a tannin-encapsulating tough hydrogel adhesive that exhibits enhanced mechanical and adhesive properties upon the encounter of leaked proteins. The hydrogel is composed of a gelatin-acrylate crosslinked network with encapsulated tannin and can adhere to a wet surface via amine-carboxyl chemistry. In the context of anastomotic leaks, tannin within the hydrogel can form a complex with proteins including the digestive enzymes, leading to increased gel stiffness and storage modulus. The enhanced mechanical strength confers improved adhesive properties on the hydrogel adhesive. Additionally, the tannin-bearing hydrogel adhesive shows excellent antibacterial properties. This adaptive and antibacterial hydrogel adhesive provides a promising sealant for gastrointestinal surgery and other applications.

Tannins↗
PubMed2025

Inflammatory pathways and immune dysregulation in pediatric postoperative septic shock: A study integrating transcriptomics, machine learning and molecular docking.

This study elucidates the molecular and immune regulatory mechanisms of pediatric postoperative septic shock. Transcriptomic data were obtained from the Gene Expression Omnibus database. Differentially expressed genes were identified using the limma package, and gene co-expression modules were constructed using Weighted Gene Co-expression Network Analysis. Functional enrichment was performed via gene set enrichment analysis, Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes analyses. Immune cell infiltration was assessed using ESTIMATE and CIBERSORT. Mendelian randomization was applied to explore causal relationships between gene expression and septic shock. Feature genes were selected using machine learning algorithms, and a diagnostic nomogram model was constructed. Finally, molecular docking analysis was performed to screen and evaluate the binding affinity of traditional Chinese medicine monomers to core target proteins. A total of 1331 differentially expressed genes were identified, and the turquoise module was strongly correlated with septic shock. Enrichment analysis revealed significant activation of IL-6/JAK/STAT3, TNF-α/NF-κB, and PI3K/Akt/mTOR pathways. Immune infiltration analysis indicated suppressed immune scores and imbalances in neutrophils, macrophages, T cells, and B cells. Mendelian randomization confirmed causal associations for 6 genes, including PIM3. The predictive model based on feature genes demonstrated high diagnostic performance. Molecular docking suggested that quercetin and astramembrannin I could stably bind PIM3. This study systematically identified core genes, dysregulated immune pathways, and candidate small-molecule interventions in pediatric septic shock, providing novel insights for early diagnosis and targeted therapy.

Humans↗
PubMed2025

RENBP inhibition amplifies metabolic glycan labeling efficiency of antigen-presenting cells in vitro and in vivo.

Metabolic glycoengineering of unnatural sugars provides a powerful tool to introduce unique chemical tags onto cell membrane for subsequent conjugation of cargos. However, the metabolic glycan labeling efficiency of antigen-presenting cells (APCs), the key mediators of adaptive immunity, is often low. Here, we report that APCs upregulate GlcNAc 2-epimerase (RENBP) and that RENBP inhibition leads to improved labeling efficiency of tetraacetyl-N-azidoacetylmannosamine (AAM) in APCs, including dendritic cells (1.2-fold), macrophages (1.3-fold), and B cells (1.4-fold) in vitro. RENBP inhibition can preferentially enhance AAM labeling efficiency in APCs than in non-APCs and selectively enhance the labeling efficiency of AAM over azido-galactosamine. We further demonstrate that RENBP inhibitors can improve AAM-mediated labeling of B cells and other APCs in vivo, with the largest enhancement for B cells (>3-fold) for 7 days. Our study uncovers a facile approach to improving metabolic glycan labeling of APCs, enabling the development of APC-targeted immunotherapies.

Animals↗
PubMed2025

Synostosis of joints caused by mutant FBN2 is linked to the abnormalities and misdifferentiation of articular surface cells.

PURPOSE: FBN2, a high-confidence effector gene for osteoarthritis (OA), was investigated for its potential role in synostosis of joints (SJ) because several OA-related genes are known to cause SJ. METHODS: We analyzed variants in OA-related genes using exome sequencing data from Chinese-Han participants with radioulnar synostosis (RUS). Variants were classified following American College of Medical Genetics and Genomics/Association for Molecular Pathology guidelines. Fbn2 knockout mice were generated via CRISPR/Cas9 and evaluated through radiological and histopathological analyses at multiple developmental stages, with complementary cellular and molecular studies. RESULTS: We identified 15 rare, damaging FBN2 variants in unrelated RUS families, including 7 likely pathogenic variants (4 null variants). Fbn2 knockout mice (both homozygous and heterozygous) exhibited SJ phenotypes. Unlike previously reported SJ mechanisms involving failed interzone formation, Fbn2-related SJ occurred after normal interzone formation. Mutant mice showed significant alterations in extracellular matrix composition and volume within articular surface cells. We proposed that these extracellular matrix changes mediated the transdifferentiation of articular surface cells into osteoblasts, which ultimately developed into bones over time. CONCLUSION: We identified FBN2 pathogenic variants that caused SJ in humans and mice. SJ caused by mutant FBN2 is linked to the abnormalities and misdifferentiation of articular surface cells.

Fibrillin-2↗
PubMed2022

Temporal associations between leukocytes DNA methylation and blood lipids: a longitudinal study.

BACKGROUND: The associations between blood lipids and DNA methylation have been investigated in epigenome-wide association studies mainly among European ancestry populations. Several studies have explored the direction of the association using cross-sectional data, while evidence of longitudinal data is still lacking. RESULTS: We tested the associations between peripheral blood leukocytes DNA methylation and four lipid measures from Illumina 450 K or EPIC arrays in 1084 participants from the Chinese National Twin Registry and replicated the result in 988 participants from the China Kadoorie Biobank. A total of 23 associations of 19 CpG sites were identified, with 4 CpG sites located in or adjacent to 3 genes (TMEM49, SNX5/SNORD17 and CCDC7) being novel. Among the validated associations, we conducted a cross-lagged analysis to explore the temporal sequence and found temporal associations of methylation levels of 2 CpG sites with triglyceride and 2 CpG sites with high-density lipoprotein-cholesterol (HDL-C) in all twins. In addition, methylation levels of cg11024682 located in SREBF1 at baseline were temporally associated with triglyceride at follow-up in only monozygotic twins. We then performed a mediation analysis with the longitudinal data and the result showed that the association between body mass index and HDL-C was partially mediated by the methylation level of cg06500161 (ABCG1), with a mediation proportion of 10.1%. CONCLUSIONS: Our study indicated that the DNA methylation levels of ABCG1, AKAP1 and SREBF1 may be involved in lipid metabolism and provided evidence for elucidating the regulatory mechanism of lipid homeostasis.

Humans↗
PubMed2007

Antiproliferation and apoptosis induction of paeonol in HepG2 cells.

AIM: To investigate the antiproliferative effect of paeonol (Pae) used alone or in combination with chemotherapeutic agents [cisplatin (CDDP), doxorubicin (DOX) and 5-fluorouracil (5-FU)] on human hepatoma cell line HepG2 and the possible mechanisms. METHODS: The cytotoxic effect of drugs on HepG2 cells was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Morphologic changes were observed by acridine orange (AO) fluorescence staining. Cell cycle and apoptosis rate were detected by flow cytometry (FCM). Drug-drug interactions were analyzed by the coefficient of drug interaction (CDI). RESULTS: Pae (7.81-250 mg/L) had an inhibitory effect on the proliferation of HepG2 cells in a dose-dependent manner, with the IC50 value of (104.77 +/- 7.28) mg/L. AO fluorescence staining and FCM assays showed that Pae induced apoptosis and arrested cell cycle at S phase in HepG2 cells. Further, different extent synergisms were observed when Pae (15.63, 31.25, 62.5 mg/L) was combined with CDDP (0.31-2.5 mg/L), DOX (0.16-1.25 mg/L), or 5-FU (12.5-100 mg/L) at appropriate concentrations. The IC50 value of the three drugs decreased dramatically when combined with Pae (P < 0.01). Of the three different combinations, the sensitivity of cells to drugs was considerably different. CONCLUSION: Pae had a significant growth-inhibitory effect on the human hepatoma cell line HepG2, which may be related to apoptosis induction and cell cycle arrest. It also can enhance the cytotoxicity of chemotherapeutic agents on HepG2 cells, and the S phase arrest induced by Pae may be one of the mechanisms of these interactions.

Acetophenones↗
PubMed2007

Detection of allelic imbalance in gene expression using pyrosequencing.

Single-nucleotide polymorphisms (SNPs) are common in the human genome, with more than 11 million SNPs having frequencies greater than 1%. The challenge is to identify the minority of functional SNPs from the large number of SNPs that are expected to be silent. Whereas coding variants are unusual, and functional (nonsynonymous) coding SNPs likely rare, regulatory SNPs appear to be common. Traditional methods to identify these SNPs in vitro are time consuming and challenging. An alternative method is to examine the allele-specific expression in the cDNA from tissues expressing the genes of interest and in individuals heterozygous for a transcribed SNP. This method permits expression to be evaluated in the context of the same trans-acting factors and to identify genes with likely cis-acting regulatory variants or parent of origin (imprinting) effects. Such studies require a method to reliably quantify the expression from each allele. Pyrosequencing offers such capabilities, and given the relatively low cost and high throughput, it offers a sensitive method to determine allelic imbalance in the cDNA from tissues expressing genes of interest.

Alleles↗
PubMed2006

The proteolytic function of the Arabidopsis 26S proteasome is required for specifying leaf adaxial identity.

Polarity formation is central to leaf morphogenesis, and several key genes that function in adaxial-abaxial polarity establishment have been identified and characterized extensively. We previously reported that Arabidopsis thaliana ASYMMERTIC LEAVES1 (AS1) and AS2 are important in promoting leaf adaxial fates. We obtained an as2 enhancer mutant, asymmetric leaves enhancer3 (ae3), which demonstrated pleiotropic plant phenotypes, including a defective adaxial identity in some leaves. The ae3 as2 double mutant displayed severely abaxialized leaves, which were accompanied by elevated levels of leaf abaxial promoting genes FILAMENTOUS FLOWER, YABBY3, KANADI1 (KAN1), and KAN2 and a reduced level of the adaxial promoting gene REVOLUTA. We identified AE3, which encodes a putative 26S proteasome subunit RPN8a. Furthermore, double mutant combinations of as2 with other 26S subunit mutations, including rpt2a, rpt4a, rpt5a, rpn1a, rpn9a, pad1, and pbe1, all displayed comparable phenotypes with those of ae3 as2, albeit with varying phenotypic severity. Since these mutated genes encode subunits that are located in different parts of the 26S proteasome, it is possible that the proteolytic function of the 26S holoenzyme is involved in leaf polarity formation. Together, our findings reveal that posttranslational regulation is essential in proper leaf patterning.

Amino Acid Sequence↗
PubMed2006

Rapid, simple, and sensitive immunoagglutination assay with SiO2 particles and quartz crystal microbalance for quantifying Schistosoma japonicum antibodies.

BACKGROUND: The resurgence of the parasitic disease schistosomiasis calls for more efficient diagnostic tests. We developed a rapid, simple, portable, and sensitive immunoagglutination assay that uses SiO(2) particles and quartz crystal microbalance (QCM) for quantifying Schistosoma japonicum (Sj) antibodies (SjAb). METHODS: We prepared submicrometer-sized silica particles derivatized with Sj antigens as replacements for traditional latex microspheres to specifically agglutinate in the presence of SjAb targets, and we used the QCM monitor to measure the resulting frequency shifts. We optimized the assay medium by adding poly(ethylene glycol) (PEG) as a response accelerator of immunoagglutination. To minimize or eliminate any nonspecific agglutination or adsorption interferences, we conducted appropriate sealing procedures separately for silica particles and the QCM probe. RESULTS: The measured frequency changes were linearly related to the SjAb concentrations in infected rabbit serum. The PEG-assisted immunoagglutination system was quantitatively sensitive to SjAb concentrations ranging from approximately 0.70 to 32.31 mg/L, with a detection limit of approximately 0.46 mg/L. The obtained linear regression equation was: y=43.61 x+80.44 (r=0.9872). Several serum specimens were evaluated with the developed QCM immunoassay and the results were compared with ELISA, validating the feasibility of practical applications. CONCLUSIONS: This novel immunoagglutination-based QCM detection format is rapid, simple to use, and more portable than conventional diagnostic immunoassays, thus offering a promising alternative tool that can be used for point-of-care clinical diagnosis of schistosomiasis, particularly in epidemic situations.

Agglutination Tests↗
PubMed2006

Oncolytic viral therapy by bladder instillation using an E1A, E1B double-restricted adenovirus in an orthotopic bladder cancer model.

OBJECTIVES: To investigate the therapeutic effect of AxdAdB-3, a double-restricted oncolytic adenovirus harboring a mutant E1A and an E1B-55KD deletion, on human bladder cancer cell lines and the SCID mouse model of orthotopic bladder cancer. METHODS: The cytopathic effects of AxdAdB-3 were evaluated in several cell lines (YTS-1, YTS-3, T24, J82, 5637) derived from human bladder or ureteral cancer and in a normal bladder mucosa-derived cell line (HCV29) with AxCAlacZ (control) or AxE1AdB (E1B-55KD-defective adenovirus) or dl922-947 (E1A-mutated adenovirus). The efficacy of bladder instillation therapy with AxdAdB-3 for orthotopic bladder cancer of SCID mice was investigated. The oncolytic effects were monitored by ultrasound examination. RESULTS: AxdAdB-3 caused the oncolysis of bladder cancer cell lines in vitro, and it was more cytopathic than AxE1AdB or dl922-947 in the cancer cell lines. AxdAdB-3 was not cytotoxic against HCV29. Direct instillation of AxdAdB-3 into the bladder of the orthotopic model inhibited tumor growth, leading to significantly prolonged survival. CONCLUSIONS: Oncolytic viral therapy delivered by instillation of AxdAdB-3 is a promising tool for treating bladder cancer.

Adenoviridae↗
PubMed2006

Expression of Nogo-A and NgR in the developing rat brain after hypoxia-ischemia.

Nogo-A and its receptor, NgR, have been shown to inhibit neurite growth in the adult rat. Therefore, we hypothesized that Nogo-A and NgR will be upregulated and thus play a similar role in the damage in developing rat brain following hypoxia-ischemia (HI). To test this hypothesis, we subjected postnatal day 7 (P7) rats to HI by permanently ligating the right common carotid artery, followed by exposure to 8%O2/92% N2 for 3 h. Rat brains at 0 h, 6 h, 12 h, 24 h and 72 h after HI, as well as from sham controls, were collected to determine histopathological damage and expression levels of Nogo-A and NgR using hematoxylin and eosin (H&E) staining, immunohistochemistry, fluorescence immunolabeling, Western blot analysis and reverse transcriptase-polymerase chain reaction (RT-PCR). We found neuronal degeneration and edema in the ischemic cortex, becoming most prominent at 24 h following HI in this model. Accordingly, the expression of Nogo-A and NgR protein was significantly upregulated at 24 h compared with the sham controls (p<0.01). The upregulated Nogo-A and NgR immunoreactive cells were mainly located in the core of the ischemic cortex and colocalized to neurons. Meanwhile, we found the expression of both Nogo-A and NgR mRNA was increased at 6 h and peaked at 12 h in the ischemic cortex after HI, compared with sham controls. Our findings of upregulation of neurite growth inhibitor Nogo-A and its receptor NgR in ischemic cortex suggest that Nogo-A and NgR may participate in the pathology seen after HI in neonatal rats.

Analysis of Variance↗
PubMed2006

Modulating cell adhesion and spreading by control of FnIII7-10 orientation on charged self-assembled monolayers (SAMs) of alkanethiolates.

In this work, we demonstrate that surface charge can be used to modulate cell adhesion/spreading through the control of the orientation of adsorbed FnIII(7-10), which is a cell-adhesive protein containing RGD residues. Carboxylic acid (COOH) and amine (NH(2))-terminated self-assembled monolayers (SAMs) of alkanethiolates were used as model negatively and positively charged surfaces, respectively. The adsorbed amount of FnIII(7-10) is controlled to be equivalent on both SAMs as confirmed by the adsorption isotherms determined using I(125)-radiolabeled FnIII(7-10.) The binding of a monoclonal antibody specific for the cell-binding domain of FnIII(7-10) was measured by surface plasmon resonance (SPR) to evaluate FnIII(7-10) orientations on different SAMs. Results indicate that adsorbed FnIII(7-10) on NH(2)-SAM has an orientation with more cell-binding domains accessible than on COOH-SAM, confirming our predictions from Monte Carlo simulations. Both phase contrast images and Vybrant MTT cell proliferation assays show that the adhesion/spreading of bovine aortic endothelial cells (BAECs) on the NH(2)-SAM is significantly better than that on the COOH-SAM coated with an equivalent amount of FnIII(7-10). These results indicate that surface charge can be used to specifically orient cell adhesive proteins such as FnIII(7-10), thus providing a promising strategy to increase the activity of materials incorporating biological moieties.

Alkanesulfonates↗
PubMed2006

Reactive oxygen species are involved in lipopolysaccharide-induced intrauterine growth restriction and skeletal development retardation in mice.

OBJECTIVE: Maternal infection is a cause of adverse developmental outcomes including embryonic resorption, intrauterine fetal death, and preterm labor. Lipopolysaccharide-induced developmental toxicity at early gestational stages has been well characterized. The purpose of the present study was to investigate the effects of maternal lipopolysaccharide exposure at late gestational stages on intrauterine fetal growth and skeletal development and to assess the potential role of reactive oxygen species in lipopolysaccharide-induced intrauterine fetal growth restriction and skeletal development retardation. STUDY DESIGN: The timed pregnant CD-1 mice were intraperitoneally injected with lipopolysaccharide (25 to 75 microg/kg per day) on gestational day 15 to 17. To investigate the role of reactive oxygen species on lipopolysaccharide-induced intrauterine fetal growth restriction and skeletal development retardation, the pregnant mice were injected with alpha-phenyl-N-t-butylnitrone (100 mg/kg, intraperitoneally) at 30 minutes before lipopolysaccharide (75 microg/kg per day, intraperitoneally), followed by an additional dose of alpha-phenyl-N-t-butylnitrone (50 mg/kg, intraperitoneally) at 3 hours after lipopolysaccharide. The number of live fetuses, dead fetuses, and resorption sites was counted on gestational day 18. Live fetuses in each litter were weighed. Crown-rump and tail lengths were examined and skeletal development was evaluated. RESULTS: Maternal lipopolysaccharide exposure significantly increased fetal mortality, reduced fetal weight and crown-rump and tail lengths of live fetuses, and retarded skeletal ossification in caudal vertebrae, anterior and posterior phalanges, and supraoccipital bone in a dose-dependent manner. Alpha-phenyl-N-t-butylnitrone, a free radical spin-trapping agent, almost completely blocked lipopolysaccharide-induced fetal death (63.2% in lipopolysaccharide group versus 6.5% in alpha-phenyl-N-t-butylnitrone + lipopolysaccharide group, P < .01). In addition, alpha-phenyl-N-t-butylnitrone significantly reversed lipopolysaccharide-induced intrauterine growth restriction and skeletal development retardation. However, aminoguanidine, a selective inhibitor of inducible nitric oxide synthase, had little effect. Furthermore, lipopolysaccharide-induced intrauterine fetal death, intrauterine fetal growth restriction, and skeletal development retardation were associated with lipid peroxidation and glutathione depletion in maternal liver, placenta, and fetal liver. Alpha-phenyl-N-t-butylnitrone significantly attenuated lipopolysaccharide-induced lipid peroxidation and glutathione depletion in maternal liver, placenta, and fetal liver. CONCLUSION: Maternal lipopolysaccharide exposure at late gestational stages results in intrauterine fetal growth restriction and skeletal development retardation in mice. Reactive oxygen species might be, at least in part, involved in lipopolysaccharide-induced intrauterine fetal growth restriction and skeletal development retardation.

Animals↗
PubMed2006

WEEE recovery strategies and the WEEE treatment status in China.

The electric and electronic equipment has been developed, applied, and consumed world wide at a very high speed. Subsequently, the ever-increasing amount of waste electric and electronic equipment (WEEE) has become a common problem facing the world. In view of the deleterious effects of WEEE on the environment and the valuable materials that can be reused in them, legislations in many countries have focused their attention on the management of WEEE, and new techniques have been developed for the recovery of WEEE. In China, rapid economic growth, coupled with urbanization and growing demand for consumer goods, has increased the consumption of EEE in large quantity, thus made the WEEE manifold rapidly, posing a severe threat to the environment and the sustainable economic growth as well. This article reviewed the implementation of strategies of WEEE treatment and the recovery technologies of WEEE. It presented the current status of WEEE and corresponding responses adopted so far in China. The concept and implementation of scientific development is critical to the sector of electronics, one of the important industrial sectors in China's economy. To achieve this objective, it is significant to recycle WEEE sufficiently to comply with regulations regarding WEEE management, and to implement green design and cleaner production concepts within the electronics industry to comply with the upcoming EU and China legislation in a proactive manner.

China↗