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学者姓名：黄明东
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Abstract ：
Vascular thiol isomerases (VTIs) encompass proteins such as protein disulfide isomerase (PDI), endoplasmic reticulum protein 5 (ERp5), ERp46, ERp57, ERp72, thioredoxin-related transmembrane protein 1 (TMX1), and TMX4, and play pivotal functions in platelet aggregation and formation of thrombosis. Investigating vascular thiol isomerases, their substrates implicated in thrombosis, the underlying regulatory mechanisms, and the development of inhibitors targeting these enzymes represents a rapidly advancing frontier within vascular biology. In this review, we summarize the structural characteristics and functional attributes of VTIs, describe the associations between these enzymes and thrombosis, and outline the progress in developing inhibitors of VTIs for potential antithrombotic therapeutic applications.
Keyword ：
Functions Functions Inhibitors Inhibitors Structures Structures Thrombosis Thrombosis Vascular thiol isomerase Vascular thiol isomerase
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| GB/T 7714 | Jiang, Longguang , Yuan, Cai , Flaumenhaft, Robert et al. Recent advances in vascular thiol isomerases: insights into structures, functions in thrombosis and antithrombotic inhibitor development [J]. | THROMBOSIS JOURNAL , 2025 , 23 (1) . |
| MLA | Jiang, Longguang et al. "Recent advances in vascular thiol isomerases: insights into structures, functions in thrombosis and antithrombotic inhibitor development" . | THROMBOSIS JOURNAL 23 . 1 (2025) . |
| APA | Jiang, Longguang , Yuan, Cai , Flaumenhaft, Robert , Huang, Mingdong . Recent advances in vascular thiol isomerases: insights into structures, functions in thrombosis and antithrombotic inhibitor development . | THROMBOSIS JOURNAL , 2025 , 23 (1) . |
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Human heavy-chain ferritin (HFn) possesses a stable and uniform cage-like structure, tumor-targeting properties, self-assembly capabilities, and biocompatibility, rendering it an ideal candidate for drug delivery. Here, we developed a dual modified HFn-based nanocage (DFn) that targets the urokinase-type plasminogen activator receptor (uPAR) and, at the same time, is responsive to the tumor microenvironment for controlled extracellular drug release. This DFn was used to co-encapsulate a photosensitizer (CPZ) and a hypoxia-activated prodrug (TPZ), creating the multifunctional nanoparticles C/T@DFn. In vitro cellular assays demonstrated that C/T@DFn significantly outperformed both unmodified HFn-based nanoparticles and its counterpart without the uPARtargeting motif in inhibiting tumor cell survival, proliferation, and migration, and showed enhanced tumor cell spheroids penetration. In vivo studies further demonstrated the improved tumor-specific accumulation and antitumor efficacy of the loaded cargo in the DFn nanocages in comparison with wild-type HFn. This improved therapeutic effect is achieved through receptor-mediated targeting and tumor microenvironment-responsive release of the cargo from the DFn nanocages, resulting in synergistic action of CPZ and TPZ within the tumor tissue. Overall, this study introduces an ideal ferritin-based nanoplatform for the efficient co-delivery of therapeutic agents, offering a promising strategy for targeted tumor therapy.
Keyword ：
Antitumor Antitumor Ferritin nanocage Ferritin nanocage uPAR-targeting uPAR-targeting
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| GB/T 7714 | Li, Hanlin , Qu, Yuhan , Guo, Zhanzhi et al. Dual modified ferritin nanocages for tumor-targeted and microenvironment-responsive drug delivery [J]. | INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES , 2025 , 303 . |
| MLA | Li, Hanlin et al. "Dual modified ferritin nanocages for tumor-targeted and microenvironment-responsive drug delivery" . | INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES 303 (2025) . |
| APA | Li, Hanlin , Qu, Yuhan , Guo, Zhanzhi , Chen, Dan , Jiang, Longguang , Xu, Peng et al. Dual modified ferritin nanocages for tumor-targeted and microenvironment-responsive drug delivery . | INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES , 2025 , 303 . |
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Angiogenesis provides essential nutrients and oxygen to tumors during tumorigenesis, facilitating invasion and metastasis. Consequently, inhibiting tumor angiogenesis is an established strategy in anti-cancer therapy. In this study, we engineered a dual-function nanosystem with both antiangiogenic and photodynamic properties. We transformed the hydrophobic photosensitizer zinc phthalocyanine (PS) into a hydrophilic form via protein renaturation, resulting in a novel photosensitizer: Monocyte-Activating Polypeptide-II (EMAP-II:PS@NPs). Characterization through dynamic light scattering (DLS) and UV-vis spectroscopy showed that these nano- particles exhibited uniform size and stability, and enhanced solubility. We further demonstrated that EMAP-II: PS@NPs effectively target tumor vascular endothelia causing intracellular photodynamic cytotoxicity. Notably, EMAP-II:PS@NPs achieved effective ablation of solid tumors at significantly reduced dosages of drugs compared to conventional therapies, due to their potent apoptotic effects on light-exposed cells. This study highlights the potential of combining anti-angiogenic activity with phototherapy, paving the way for innovative cancer treatment strategies.
Keyword ：
Angiogenesis Angiogenesis Anti-tumor Anti-tumor EMAP-II EMAP-II Phthalocyanine Phthalocyanine
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| GB/T 7714 | Chen, Liyun , Li, Linlin , Zhao, Hailong et al. Integration of EMAP-II-targeted anti-angiogenesis and photodynamic therapy using zinc phthalocyanine nanosystem for enhanced cancer treatment [J]. | COLLOIDS AND SURFACES B-BIOINTERFACES , 2025 , 248 . |
| MLA | Chen, Liyun et al. "Integration of EMAP-II-targeted anti-angiogenesis and photodynamic therapy using zinc phthalocyanine nanosystem for enhanced cancer treatment" . | COLLOIDS AND SURFACES B-BIOINTERFACES 248 (2025) . |
| APA | Chen, Liyun , Li, Linlin , Zhao, Hailong , Li, Hao , Li, Jiahui , Li, Chao et al. Integration of EMAP-II-targeted anti-angiogenesis and photodynamic therapy using zinc phthalocyanine nanosystem for enhanced cancer treatment . | COLLOIDS AND SURFACES B-BIOINTERFACES , 2025 , 248 . |
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The angiopoietin (Ang)-Tie axis, critical for endothelial cell function and vascular development, is a promising therapeutic target for treating vascular disorders and inflammatory conditions like sepsis. This study aimed to enhance the binding affinity of recombinant Ang1 variants to the Tie2 and explore their therapeutic potential. Structural insights from the Ang1-Tie2 complex enabled the identification of key residues within the Ang1 receptor binding domain (RBD) critical for Tie2 interaction. Molecular dynamics simulations revealed that Met436Arg (M436R) and Ala451Asp (A451D) could improve Ang1's Tie2 binding affinity. One variant, Ang1-RBDA451D, demonstrated a 100-fold increase compared to the wild type. Cellular assays revealed that Ang1A451D enhanced Tie2 phosphorylation, promoting endothelial cell migration and tube formation. In vivo, this variant effectively reduced inflammatory cytokines and attenuated organ damage in septic mice. These findings highlight Ang1A451D as a promising therapeutic candidate for vascular diseases, offering notable clinical potential for mitigating sepsis-related vascular dysfunction.
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| GB/T 7714 | Wang, Rui , Li, Hao , Xie, Zhinuo et al. Development of a recombinant Ang1 variant with enhanced Tie2 binding and its application to attenuate sepsis in mice [J]. | SCIENCE ADVANCES , 2025 , 11 (3) . |
| MLA | Wang, Rui et al. "Development of a recombinant Ang1 variant with enhanced Tie2 binding and its application to attenuate sepsis in mice" . | SCIENCE ADVANCES 11 . 3 (2025) . |
| APA | Wang, Rui , Li, Hao , Xie, Zhinuo , Huang, Meijuan , Xu, Peng , Yuan, Cai et al. Development of a recombinant Ang1 variant with enhanced Tie2 binding and its application to attenuate sepsis in mice . | SCIENCE ADVANCES , 2025 , 11 (3) . |
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Aims Alteplase is a cornerstone thrombolytic agent in clinical practice but presents a potential bleeding risk. Stroke patients need pre-screening to exclude haemorrhagic stroke before using alteplase. In this study, we develop a new thrombolytic agent citPA5, characterized by an enhanced safety profile and minimal bleeding tendency.Methods and results A clot lysis agent, named citPA5, is developed based on rtPA with point mutations to completely suppress its proteolytic activity in the absence of fibrin. In the presence of fibrin, citPA5 exhibited significantly higher fibrinolytic activity (a 15.8-fold increase of kcat/Km). Furthermore, citPA5 showed resistance to endogenous fibrinolysis inhibitor, PAI-1, resulting in enhanced potency. In a series of safety evaluation experiments, including thrombelastography assay, mice tail bleeding assay, and a murine intracerebral haemorrhage (ICH) model, citPA5 did not cause systemic bleeding or worsen ICH compared with alteplase. This highlights the low risk of bleeding associated with citPA5. Finally, we found that citPA5 effectively improved cerebral blood flow and reduced infarct volume in a carotid embolism-induced stroke model.Conclusion This clot lysis agent, citPA5, not only exhibits a low risk of bleeding but also demonstrates highly effective thrombolysis capabilities. As a result, citPA5 shows great potential for administration prior to the classification of stroke types, making it possible for use in ambulances at the onset of stroke when symptoms are identified. The findings presented in this study also suggest that this strategy could be applied to develop a new generation of fibrinolytic drugs that offer greater safety and specificity in targeting fibrin. Graphical Abstract
Keyword ：
Enhanced tPA potency Enhanced tPA potency Ischaemic stroke Ischaemic stroke Low bleeding risk Low bleeding risk Thrombolytic therapy Thrombolytic therapy
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| GB/T 7714 | Chen, Shanli , Fang, Sudan , Zhou, Yang et al. A low bleeding risk thrombolytic agent: citPA5 [J]. | CARDIOVASCULAR RESEARCH , 2024 , 120 (10) : 1191-1201 . |
| MLA | Chen, Shanli et al. "A low bleeding risk thrombolytic agent: citPA5" . | CARDIOVASCULAR RESEARCH 120 . 10 (2024) : 1191-1201 . |
| APA | Chen, Shanli , Fang, Sudan , Zhou, Yang , Huang, Zhiwei , Yu, Shujuan , Chen, Dan et al. A low bleeding risk thrombolytic agent: citPA5 . | CARDIOVASCULAR RESEARCH , 2024 , 120 (10) , 1191-1201 . |
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BACKGROUND:Integrins mediate the adhesion, crawling, and migration of neutrophils during vascular inflammation. Thiol exchange is important in the regulation of integrin functions. ERp72 (endoplasmic reticulum-resident protein 72) is a member of the thiol isomerase family responsible for the catalysis of disulfide rearrangement. However, the role of ERp72 in the regulation of Mac-1 (integrin alpha M beta 2) on neutrophils remains elusive.METHODS:Intravital microscopy of the cremaster microcirculation was performed to determine in vivo neutrophil movement. Static adhesion, flow chamber, and flow cytometry were used to evaluate in vitro integrin functions. Confocal fluorescent microscopy and coimmunoprecipitation were utilized to characterize the interactions between ERp72 and Mac-1 on neutrophil surface. Cell-impermeable probes and mass spectrometry were used to label reactive thiols and identify target disulfide bonds during redox exchange. Biomembrane force probe was performed to quantitatively measure the binding affinity of Mac-1. A murine model of acute lung injury induced by lipopolysaccharide was utilized to evaluate neutrophil-associated vasculopathy.RESULTS:ERp72-deficient neutrophils exhibited increased rolling but decreased adhesion/crawling on inflamed venules in vivo and defective static adhesion in vitro. The defect was due to defective activation of integrin Mac-1 but not LFA-1 (lymphocyte function-associated antigen-1) using blocking or epitope-specific antibodies. ERp72 interacted with Mac-1 in lipid rafts on neutrophil surface leading to the reduction of the C654-C711 disulfide bond in the alpha M subunit that is critical for Mac-1 activation. Recombinant ERp72, via its catalytic motifs, increased the binding affinity of Mac-1 with ICAM-1 (intercellular adhesion molecule-1) and rescued the defective adhesion of ERp72-deficient neutrophils both in vitro and in vivo. Deletion of ERp72 in the bone marrow inhibited neutrophil infiltration, ameliorated tissue damage, and increased survival during murine acute lung injury.CONCLUSIONS:Extracellular ERp72 regulates integrin Mac-1 activity by catalyzing disulfide rearrangement on the alpha M subunit and may be a novel target for the treatment of neutrophil-associated vasculopathy.
Keyword ：
disulfides disulfides ERp72 ERp72 isomerases isomerases macrophage-1 antigen macrophage-1 antigen microscopy microscopy neutrophil infiltration neutrophil infiltration neutrophils neutrophils
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| GB/T 7714 | Li, Yaofeng , Xu, Xulin , Wang, Haoqing Jerry et al. Endoplasmic Reticulum Protein 72 Regulates Integrin Mac-1 Activity to Influence Neutrophil Recruitment [J]. | ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY , 2024 , 44 (3) : E82-E98 . |
| MLA | Li, Yaofeng et al. "Endoplasmic Reticulum Protein 72 Regulates Integrin Mac-1 Activity to Influence Neutrophil Recruitment" . | ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY 44 . 3 (2024) : E82-E98 . |
| APA | Li, Yaofeng , Xu, Xulin , Wang, Haoqing Jerry , Chen, Yiyao Catherine , Chen, Yaobing , Chiu, Joyce et al. Endoplasmic Reticulum Protein 72 Regulates Integrin Mac-1 Activity to Influence Neutrophil Recruitment . | ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY , 2024 , 44 (3) , E82-E98 . |
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Using copper-ionophores to translocate extracellular copper into mitochondria is a clinically validated anticancer strategy that has been identified as a new type of regulated cell death termed "cuproptosis." This study reports a mitochondria-targeting Cu(I) complex, Cu(I)Br(PPh3)(3) (CBP), consisting of a cuprous ion coordinated by three triphenylphosphine moieties and a Br atom. CBP exhibited antitumor and antimetastatic efficacy in vitro and in vivo by specifically targeting mitochondria instigating mitochondrial dysfunction. The cytotoxicity of CBP could only be reversed by a copper chelator rather than inhibitors of the known cell death, indicating copper-dependent cytotoxicity. Furthermore, CBP induced the oligomerization of lipoylated proteins and the loss of Fe-S cluster proteins, consistent with characteristic features of cuproptosis. Additionally, CBP induced remarkable intracellular generation of reactive oxygen species (ROS) through a Fenton-like reaction, indicating a complex antitumor mechanism. This is a proof-of-concept study exploiting the antitumor activity and mechanism of the Cu(I)-based mitochondria-targeting therapy.
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| GB/T 7714 | Xu, Siyu , Hao, Yashuai , Xu, Xinyi et al. Antitumor Activity and Mechanistic Insights of a Mitochondria-Targeting Cu(I) Complex [J]. | JOURNAL OF MEDICINAL CHEMISTRY , 2024 , 67 (10) : 7911-7920 . |
| MLA | Xu, Siyu et al. "Antitumor Activity and Mechanistic Insights of a Mitochondria-Targeting Cu(I) Complex" . | JOURNAL OF MEDICINAL CHEMISTRY 67 . 10 (2024) : 7911-7920 . |
| APA | Xu, Siyu , Hao, Yashuai , Xu, Xinyi , Huang, Lu , Liang, Yuqiong , Liao, Jia et al. Antitumor Activity and Mechanistic Insights of a Mitochondria-Targeting Cu(I) Complex . | JOURNAL OF MEDICINAL CHEMISTRY , 2024 , 67 (10) , 7911-7920 . |
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Bacterial infections of plants are widespread and highly virulent, causing serious economic losses in agricultural production worldwide. These infections become particularly prevalent during rainy weather, characterized by high humidity and low light intensity (about 2-10% of a sunny day). Here we identified a class of photosensitizers that were effective in inhibiting plant bacterial infections under rainy weather with dim light. One of these compounds, compound 1, demonstrated exceptional efficacy by eliminating more than 4 logs (99.99%) of either Xanthomonas perforans or Xanthomonas citri subsp. citri (Xcc) strain at a concentration of 6.25 mu M under rainy weather conditions with a light exposure of 28.51 J/cm2. For Clavibacter michiganensis (Cm), compound 1 demonstrated a comparable bactericidal effect at a lower concentration of 3.13 mu M. Furthermore, compound 1 was effective in controlling plant leaf infections during rainy weather. Moreover, compound 1 exhibited a potent inhibitory effect on the biofilms pertinent to tomato spot disease and citrus canker under natural illumination on rainy days. Additionally, compound 1 displayed remarkable resilience to rain-wash on plant leaves, retaining 41.20% of its initial concentration following exposure to three simulated rain events. These findings provide a new strategy for plant pathogen disease management highlight its feasibility even during rainy weather.
Keyword ：
Biofilm Biofilm Photosensitizer Photosensitizer Plant bacterial infection Plant bacterial infection Rain fastness Rain fastness
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| GB/T 7714 | Wang, Guodong , Li, Jiahui , Zhang, Wei et al. A class of photosensitizer highly effective to control bacterial infection in plants even on rainy days with dim light [J]. | DYES AND PIGMENTS , 2024 , 225 . |
| MLA | Wang, Guodong et al. "A class of photosensitizer highly effective to control bacterial infection in plants even on rainy days with dim light" . | DYES AND PIGMENTS 225 (2024) . |
| APA | Wang, Guodong , Li, Jiahui , Zhang, Wei , Jiang, Libin , Mai, Yuhan , Chen, Jingyi et al. A class of photosensitizer highly effective to control bacterial infection in plants even on rainy days with dim light . | DYES AND PIGMENTS , 2024 , 225 . |
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Polyoxometalates (POMs) are a class of anionic metal-oxygen clusters with versatile biological activities. Over the past decade, an increasing number of POMs, especially Sb-rich POMs, have been proven to exert antitumor activity. However, the antitumor effects and mechanisms of POMs in the treatment of non-small cell lung cancer (NSCLC) remain largely unexplored. This study employed a Sb-rich {Sb21Tb7W56} POM (POM-1) for NSCLC therapy and investigated its mechanism of action. Our results demonstrated that POM-1 exhibited cytotoxicity against H1299 and A549 cells with IC50 values of 3.245 mu M and 3.591 mu M, respectively. The migration and invasion were also inhibited by 28.05% and 76.18% in H1299 cells, as well as 36.88% and 36.98% in A549 cells at a concentration of 5 mu M. In a tumor xenograft mouse model, POM-1 suppressed tumor growth by 76.92% and 84.62% at doses of 25 and 50 mg kg-1, respectively. Transcriptomic analysis indicated the alteration of ferroptosis and apoptosis signaling pathways in POM-treated NSCLC cells. Subsequent experimentation confirmed the induction of ferroptosis, evidenced by 5.6-fold elevated lipid peroxide levels with treatment of 5 mu M POM-1, alongside increased expression of ferroptosis-associated proteins. Additionally, the apoptosis induced by POM-1 was also validated by the 19.67% and 30.1% increase in apoptotic cells in H1299 and A549 cells treated with 5 mu M POM-1, respectively, as well as the upregulated activation of caspase-3. In summary, this study reveals, for the first time, ferroptosis as the antitumor mechanism of Sb-rich POM, and that synergism with ferroptosis and apoptosis is a highly potent antitumor strategy for POM-based antitumor therapy. This study first reveals the ferroptosis antitumor mechanism of a Sb-rich polyoxometalate (POM) for non-small cell lung cancer therapy and demonstrates ferroptosis and apoptosis as a highly potent antitumor strategy for POM-based antitumor therapy.
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| GB/T 7714 | Lin, Jie-Wei , Zhou, Yang , Xiao, Hui-Ping et al. Antitumor effects of a Sb-rich polyoxometalate on non-small-cell lung cancer by inducing ferroptosis and apoptosis [J]. | CHEMICAL SCIENCE , 2024 , 15 (37) : 15367-15376 . |
| MLA | Lin, Jie-Wei et al. "Antitumor effects of a Sb-rich polyoxometalate on non-small-cell lung cancer by inducing ferroptosis and apoptosis" . | CHEMICAL SCIENCE 15 . 37 (2024) : 15367-15376 . |
| APA | Lin, Jie-Wei , Zhou, Yang , Xiao, Hui-Ping , Wu, Lei-Lei , Li, Peng-Cheng , Huang, Ming-Dong et al. Antitumor effects of a Sb-rich polyoxometalate on non-small-cell lung cancer by inducing ferroptosis and apoptosis . | CHEMICAL SCIENCE , 2024 , 15 (37) , 15367-15376 . |
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Serine proteases, a significant class of enzymes comprising approximately one-third of known human proteases, are ubiquitously present across various organisms. These enzymes typically exhibit highly conserved catalytic domain structures, and their activity is stringently regulated within the body, playing a pivotal role in numerous physiological processes. Dysregulation of serine protease activity can result in severe consequences, including excessive inflammation, heightened risk of thrombosis and cancer, and even mortality. Serine protease inhibitors have emerged as critical regulators, offering a broad range of physiological functions such as maintaining the coagulation-fibrinolysis balance, modulating inflammatory responses, accelerating wound healing, promoting apoptosis, and providing antitumor and antiviral effects. As a result, the development of serine protease inhibitors has become increasingly vital. In recent years, significant progress in the study of serine proteases has led to the pivotal role of various serine protease inhibitors in clinical diagnosis and treatment. This review explores the fundamental mechanisms of serine protease inhibitors, summarizes those that have been successfully integrated into clinical practice, and discusses the challenges encountered in their development along with partial solutions. These advancements lay the groundwork for further refinement and innovation in serine protease inhibitor therapeutics.
Keyword ：
challenges challenges clinical application clinical application serine protease serine protease serine protease inhibitor serine protease inhibitor strategies strategies
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| GB/T 7714 | Wei, Yang , Huang, Mingdong , Jiang, Longguang . Advancements in Serine Protease Inhibitors: From Mechanistic Insights to Clinical Applications [J]. | CATALYSTS , 2024 , 14 (11) . |
| MLA | Wei, Yang et al. "Advancements in Serine Protease Inhibitors: From Mechanistic Insights to Clinical Applications" . | CATALYSTS 14 . 11 (2024) . |
| APA | Wei, Yang , Huang, Mingdong , Jiang, Longguang . Advancements in Serine Protease Inhibitors: From Mechanistic Insights to Clinical Applications . | CATALYSTS , 2024 , 14 (11) . |
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