an-atherosclerosis-model-mice-induced-both-partial-carotid-ligation

An Atherosclerosis Model in Mice Induced by Both Partial Carotid Ligation and Overexpression of <em>PCSK9</em>

The lack of rapid, reproducible carotid-specific atherosclerosis models in wild-type mice limits translational studies of plaque biology and therapies. ...

identification-hub-genes-single-nucleotide-polymorphisms-potential

Identification of Hub Genes, Single-Nucleotide Polymorphisms, and Potential Drug Targets In Breast Cancer Using Transcriptomic Analysis

HER2-positive (HER2+) breast cancer often develops resistance to therapies like Lapatinib, potentially involving mitochondrial metabolic and redox ...

Chinese Academy of Medical Sciences and Peking Union Medical College

The Affiliated Hospital of Xuzhou Medical University

Vaspin (visceral adipose tissue-derived serine protease inhibitor) is a recently discovered adipokine that has been implicated in diabetes mellitus and other metabolic disorders. However, the effects of vaspin on pancreatic β cell function and related mechanisms are not fully understood. Thus, the present study was performed to investigate the effects of vaspin on pancreatic β cell function and the potential underlying mechanisms. Both in vitro (rat insulinoma cells, INS-1) and in vivo (high fat diet fed rats) experiments were conducted. The results showed that vaspin significantly increased INS-1 cell secretory function. Potential mechanisms were explored using inhibitors, western blot and real-time PCR techniques. We found that vaspin increased the levels of IRS-2 mRNA and IRS-2 total protein, while decreased the serine phosphorylation level of IRS-2 protein. Moreover, vaspin increased the Akt phosphorylation protein level which was reversed by PI3K inhibitor ly294002. In addition, vaspin increased the phosphorylation levels of mTOR and p70S6K, which was inhibited by rapamycin. Meanwhile, we found that the NF-κB mRNA and protein levels were reduced after vaspin treatment, similar to the effect of NF-κB inhibitor TPCK. Furthermore, vaspin increased the glucose stimulated insulin secretion (GSIS) level, lowered blood glucose level and improved the glucose tolerance and insulin sensitivity of high fat diet fed rats. Hyperglycemic clamp test manifested that vaspin improved islet β cell function. Together, these findings provide a new understanding of the function of vaspin on pancreatic β cell and suggest that it may serve as a potential agent for the prevention and treatment of type 2 diabetes.

Effects of vaspin on pancreatic β cell secretion via PI3K/Akt and NF-κB signaling pathways.

Insulin resistance (IR) is the main pathogenesis of metabolic syndrome and a shared pathophysiological change in conditions such as diabetes mellitus, adiposity, hypertension, and atherosclerosis. Visceral adipose tissue-derived serpin (Vaspin) is a newly discovered adipocytokine with insulin-sensitizing and anti-inflammatory effects. To examine if vaspin can improve insulin resistance in rats fed a high-fat diet via the insulin receptor substrate/phosphatidylinositol 3 kinase/protein kinase B/glucose transport (IRS/PI3K/Akt/Glut) and inhibitory κB alpha/nuclear factor-kappa B (IκBα/NF-κB) signalling pathways, thirty male Sprague-Dawley (SD) rats were randomly divided into three groups: the normal control group (NC group, n = 10), high-fat diet group (HFD group, n = 10) and vaspin intervention group (HFD + vaspin group, n = 10). Results showed that intervention with vaspin significantly decreased fasting blood glucose (FBG) and fasting insulin (FINS) concentrations in HFD - fed rats without significantly affecting body weight or triglyceride (TG) or total cholesterol (TC) levels. The areas under the intraperitoneal glucose tolerance test (IPGTT) and the insulin tolerance test (ITT) curves were significantly decreased in HFD + vaspin group compared with the HFD group, and the glucose infusion rate (GIR) showed the same trends. Western blot, real-time polymerase chain reaction (RT-PCR) and immunofluorescence staining showed that vaspin could improve insulin resistance in liver, skeletal muscle and adipose tissue by activating the IRS/PI3K/Akt/Glut signalling pathway and inhibiting the IκBα/NF-κB signalling pathway.

Effects of Vaspin on Insulin Resistance in Rats and Underlying Mechanisms.

To describe the genetic landscape and clinical characteristics of Chinese patients diagnosed with papillary thyroid cancer (PTC) and to determine which high-risk genetic characteristics suggest a likelihood of lymph node metastasis (LNM) and lateral lymph node metastasis (LLNM).

Genetic and Clinicopathologic Characteristics of Papillary Thyroid Carcinoma in the Chinese Population: High  Mutation Allele Frequency, Multiple Driver Gene Mutations, and  Fusion May Indicate More Advanced TN Stage.

For developing an effective interventional approach and treatment modality for PM2.5, the effects of omega-3 fatty acids on alleviating inflammation and attenuating lung injury induced by inhalation exposure of PM2.5 were assessed in murine models. We found that daily oral administration of the active components of omega-3 fatty acids, docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA) effectively alleviated lung parenchymal lesions, restored normal inflammatory cytokine levels and oxidative stress levels in treating mice exposed to PM2.5 (20 mg/kg) every 3 days for 5 times over a 14-day period. Especially, CT images and the pathological analysis suggested protective effects of DHA and EPA on lung injury. The key molecular mechanism is that DHA and EPA can inhibit the entry and deposition of PM2.5, and block the PM2.5-mediated cytotoxicity, oxidative stress, and inflammation.

Oral Administration of Omega-3 Fatty Acids Attenuates Lung Injury Caused by PM2.5 Respiratory Inhalation Simply and Feasibly In Vivo.

In this study, we aimed to investigate the classification of symptomatic plaques by evaluating the models generated via two different approaches, a radiomics-based machine learning (ML) approach, and an end-to-end learning approach which utilized deep learning (DL) techniques with several representative model frameworks.

Radiomics and artificial neural networks modelling for identification of high-risk carotid plaques.

Abdominal aortic aneurysm (AAA) is a degenerative disease that caused mortality in people aged >65. Senescence plays a critical role in AAA pathogenesis. Advances in AAA repair techniques have occurred, but a remaining priority is therapies to limit AAA growth and rupture. Our Previous study found cyclic nucleotide phosphodiesterase 1C (PDE1C) exacerbate AAA through aggravate vascular smooth muscle cells (VSMCs) senescence by downregulating Sirtuin1 (SIRT1) expression and activity. Vinpocetine as a selective inhibitor of PDE1 and a clinical medication for cerebral vasodilation, it is unclear whether vinpocetine can rely on SIRT1 to alleviate AAA. This study showed that pre-treatment with vinpocetine remarkably prevented aneurysmal dilation and reduced aortic rupture in elastase-induced AAA mice. In addition, the elastin degradation, MMP (matrix metalloproteinase) activity, macrophage infiltration, ROS production, collagen fibers remodeling, and VSMCs senescence were decreased in AAA treated with vinpocetine. While these effects were unable to exert in VSMCs-specific SIRT1 knockout AAA mice. Accordingly, we revealed that vinpocetine suppressed migration, proliferation, and senescence in VSMCs. Moreover, vinpocetine reduced SIRT1 degradation by inhibiting lysosome-mediated autophagy. In conclusion, this study indicated that vinpocetine may be as a potential drug for therapy AAA through alleviate VSMCs senescence via the SIRT1-dependent pathway.

Vinpocetine alleviates the abdominal aortic aneurysm progression via VSMCs SIRT1-p21 signaling pathway.

Non-pharmacological interventions (NPIs) are recommended in current international clinical practice guidelines for the management of axial spondyloarthritis (axSpA) as a complementary therapy.

Non-pharmacological interventions for patients with axial spondyloarthritis: a meta-analysis.

HER2-positive breast cancer was aggressive, resulting in a poorer prognosis. This multicenter study analyzed the real-world data of women treated with pyrotinib-based therapy, aiming to describe their characteristics, treatment regimens, and to investigate the clinical outcomes.

Pyrotinib in the Treatment of Women With HER2-Positive Advanced Breast Cancer: A Multicenter, Prospective, Real-World Study.

Recent studies in the United States have shown that breast cancer accounts for 30% of all new cancer diagnoses in women and has become the leading cause of cancer deaths in women worldwide. Chondroitin Polymerizing Factor (CHPF), is an enzyme involved in chondroitin sulfate (CS) elongation and a novel key molecule in the poor prognosis of many cancers. However, its role in the development and progression of breast cancer remains unclear.

Bioinformatics and Experimental Analysis of the Prognostic and Predictive Value of the CHPF Gene on Breast Cancer.

Natural killer (NK) cells are crucial to cancer development and prognosis. However, the role of NK cell-related genes in immunotherapy and the tumor immune microenvironment (TIME) is not well understood. This study aimed to develop reliable risk signatures associated with NK cell-related genes for predicting thyroid cancer (THCA).

Prognosis and therapy in thyroid cancer by gene signatures related to natural killer cells.

Zinc oxide nanoparticles (ZnO NPs) stand as among the most significant metal oxide nanoparticles in trigger the formation of reactive oxygen species (ROS) and induce apoptosis. Nevertheless, the utilization of ZnO NPs has been limited by the shallowness of short-wavelength light and the constrained production of ROS. To overcome these limitations, a strategy involves achieving a red shift towards the near-infrared (NIR) light spectrum, promoting the separation and restraining the recombination of electron-hole (e-h) pairs. Herein, the hybrid plasmonic system Au@ZnO (AZ) with graphene quantum dots (GQDs) doping (AZG) nano heterostructures is rationally designed for optimal NIR-driven cancer treatment. Significantly, a multifold increase in ROS generation can be achieved through the following creative initiatives: (i) plasmonic Au nanorods expands the photocatalytic capabilities of AZG into the NIR domain, offering a foundation for NIR-induced ROS generation for clinical utilization; (ii) elaborate design of mesoporous core-shell AZ structures facilitates the redistribution of electron-hole pairs; (iii) the incorporation GQDs in mesoporous structure could efficiently restrain the recombination of the e-h pairs; (iv) Modification of hyaluronic acid (HA) can enhance CD44 receptor mediated targeted triple-negative breast cancer (TNBC). In addition, the introduced Au NRs present as catalysts for enhancing photothermal therapy (PTT), effectively inducing apoptosis in tumor cells. The resulting HA-modified AZG (AZGH) exhibits efficient hot electron injection and e-h separation, affording unparalleled convenience for ROS production and enabling NIR-induced PDT for the cancer treanment. As a result, our well-designed mesoporous core-shell AZGH hybrid as photosensitizers can exhibit excellent PDT efficacy.

Ternary heterostructure-driven photoinduced electron-hole separation enhanced oxidative stress for triple-negative breast cancer therapy.

Human L35a ribosomal protein (RPL35A) has been reported to confer higher drug resistance and viability to triple-negative breast cancer (TNBC) cells, but the mechanism related to its promotion of TNBC malignant progression is still unclear. Here, we found that silencing of RPL35A could inhibit the proliferation of TNBC cells by suppressing the G1/S phase transition. Furthermore, SMAD-specific E3 ubiquitin protein ligase 2 (Smurf2) was found to be a potential upstream ubiquitin ligase of RPL35A. Smurf2 could interact with RPL35A and promote its degradation and K63-linked polyubiquitination, thereby suppressing the G1/S phase transition and proliferation of TNBC cells. In addition, the roles of Smurf2 were confirmed in a xenograft mouse model. Finally, we found a negative correlation between the protein levels of RPL35A and Smurf2 in human TNBC tissues. In summary, Smurf2 inhibits the proliferation of TNBC cells by blocking the cell cycle process, which is associated with regulating RPL35A.

ArticleTotal : 2	Year
Publication title	2026
Publication title	2026

Article	Year
Effects of vaspin on pancreatic β cell secretion via PI3K/Akt and NF-κB signaling pathways. PloS one\| PubMed ID: 29240812	2017
Effects of Vaspin on Insulin Resistance in Rats and Underlying Mechanisms. Scientific reports\| PubMed ID: 30202052	2018
Genetic and Clinicopathologic Characteristics of Papillary Thyroid Carcinoma in the Chinese Population: High Mutation Allele Frequency, Multiple Driver Gene Mutations, and Fusion May Indic... OncoTargets and therapy\| PubMed ID: 35173448	2022
Oral Administration of Omega-3 Fatty Acids Attenuates Lung Injury Caused by PM2.5 Respiratory Inhalation Simply and Feasibly In Vivo. International journal of molecular sciences\| PubMed ID: 35628131	2022
Radiomics and artificial neural networks modelling for identification of high-risk carotid plaques. Frontiers in cardiovascular medicine\| PubMed ID: 37485276	2023
Vinpocetine alleviates the abdominal aortic aneurysm progression via VSMCs SIRT1-p21 signaling pathway. Acta pharmacologica Sinica\| PubMed ID: 39179867	2025
Non-pharmacological interventions for patients with axial spondyloarthritis: a meta-analysis. Therapeutic advances in musculoskeletal disease\| PubMed ID: 40183114	2025
Pyrotinib in the Treatment of Women With HER2-Positive Advanced Breast Cancer: A Multicenter, Prospective, Real-World Study. Frontiers in oncology\| PubMed ID: 34336688	2021
Bioinformatics and Experimental Analysis of the Prognostic and Predictive Value of the CHPF Gene on Breast Cancer. Frontiers in oncology\| PubMed ID: 35372047	2022
Prognosis and therapy in thyroid cancer by gene signatures related to natural killer cells. The journal of gene medicine\| PubMed ID: 38282150	2024
Ternary heterostructure-driven photoinduced electron-hole separation enhanced oxidative stress for triple-negative breast cancer therapy. Journal of nanobiotechnology\| PubMed ID: 38735931	2024
Smurf2 Suppresses Proliferation and Cell Cycle of Triple-Negative Breast Cancer Cells by Promoting the Polyubiquitination and Degradation of RPL35A. Journal of cellular and molecular medicine\| PubMed ID: 39871432	2025

Jiaxin Zhang

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