Shao‐ling Yang  Lv‐yun Zhu  Rui Han  Lei‐lei Sun  Jun‐xia Li  Jing‐tao Dou 《Journal of Diabetes》2017,9(2):133-140

Peripheral arterial disease (PAD) increases the risk of lower extremity amputation. It is also an independent predictor of cardiovascular and cerebrovascular ischemic events, affecting both the quality and expectancy of life. Many studies have demonstrated that the prevalence of PAD in patients with diabetes mellitus (DM) is higher than in non‐diabetic patients. In diabetic patients, PAD occurs early with rapid progression, and is frequently asymptomatic. Multiple metabolic aberrations in DM, such as advanced glycation end‐products, low‐density lipoprotein cholesterol, and abnormal oxidative stress, have been shown to worsen PAD. However, the role of DM in PAD is not completely understood. The purpose of the present article is to review and discuss the pathophysiology of PAD in DM.  相似文献   

    

Xiaoping Chen  Xiaofeng Lv  Gangyi Yang  Dan Lu  Chunli Piao  Xiaomei Zhang  Hong Jiang  Ying Xie  Jinkui Yang  Xuefeng Li  Yanbing Li  Xinhua Xiao  Yukun Li  Li Sun  Shaoxiong Zheng  Qingfeng Cheng  Yongde Peng  Wenying Yang 《Journal of Diabetes》2017,9(2):158-167

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Ying Yang  Xiqing Rong  Xue Lv  Wenbing Jiang  Yuan Yang  Dongwu Lai  Shiming Xu  Guosheng Fu 《Cardiovascular therapeutics》2017,35(5)

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Pingping Zhang  Qiuxia Li  Jun Qi  Qing Lv  Xuqi Zheng  Xinyu Wu  Jieruo Gu 《International journal of rheumatic diseases》2017,20(10):1510-1516

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Padmaja Sankaridurg  Xiangui He  Thomas Naduvilath  Minzhi Lv  Arthur Ho  Earl Smith III  Paul Erickson  Jianfeng Zhu  Haidong Zou  Xun Xu 《Acta ophthalmologica. Supplement》2017,95(7):e633-e640

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Na Yang  Lu Lv  Shu-Meng Han  Li-Yun He  Zi-Yi Li  Yu-Cheng Yang  Fan Ping  Ling-Ling Xu  Wei Li  Hua-Bing Zhang  Yu-Xiu Li 《World journal of diabetes》2025,16(1)

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Shan Shan  Yan Li  Jingjing Wang  Zhe Lv  Dawei Yi  Qiong Huang  Chris J. Corrigan  Wei Wang  Zhang Quangeng  Sun Ying 《Immunology》2016,148(1):83-91

The T‐helper cell type 2‐promoting cytokine interleukin‐33 (IL‐33) has been implicated in asthma pathogenesis. Angiogenesis is a feature of airways remodelling in asthma. We hypothesized that IL‐33 induces airways angiogenesis and expression of angiogenic factors in an established murine surrogate of asthma. In the present study, BALB/c mice were subjected to serial intranasal challenge with IL‐33 alone for up to 70 days. In parallel, ovalbumin (OVA) ‐sensitized mice were subjected to serial intranasal challenge with OVA or normal saline to serve as positive and negative controls, respectively. Immunohistochemical analysis of expression of von Willebrand factor and erythroblast transformation‐specific‐related gene, both blood vessel markers, and angiogenic factors angiogenin, insulin‐like growth factor‐1, endothelin‐1, epidermal growth factor and amphiregulin was performed in lung sections ex vivo. An established in‐house assay was used to test whether IL‐33 was able to induce microvessel formation by human vascular endothelial cells. Results showed that serial intranasal challenge of mice with IL‐33 or OVA resulted in proliferation of peribronchial von Willebrand factor‐positive blood vessels to a degree closely related to the total expression of the angiogenic factors amphiregulin, angiogenin, endothelin‐1, epidermal growth factor and insulin‐like growth factor‐1. IL‐33 also induced microvessel formation by human endothelial cells in a concentration‐dependent fashion in vitro. Our data are consistent with the hypothesis that IL‐33 has the capacity to induce angiogenesis at least partly by increasing local expression of multiple angiogenic factors in an allergen‐independent murine asthma surrogate, and consequently that IL‐33 or its receptor is a potential novel molecular target for asthma therapy.  相似文献   

    

Yang Liu  Huilin Lv  Li Ren  Yingjun Wang 《Journal of biomaterials science. Polymer edition》2016,27(8):758-772

Cornea disease is the second cause of blindness and keratoplasty is the most commonly performed option for visual rehabilitation of patients with corneal blindness. However, the clinical treatment has been drastically limited due to a severe shortage of high-quality donor corneas. Although collagen film with outstanding biocompatibility has promising application in corneal tissue engineering, the moisturizing properties of collagen-based materials must be further improved to satisfy the requirements of clinical applications. This paper describes a novel collagen-based film with high moisture capacity reinforced by surface grafting of chondroitin sulfate. The collagen-chondroitin sulfate (abbreviated as Col-CS) film was analyzed by Fourier transform infrared spectroscopy and X-ray photoelectron spectroscopy and its hydrophilic property, moisture retention, optical property, and mechanical performance had been tested. The moisture-retaining capacity is found to be improved with the introduction of chondroitin sulfate, and the Col-CS membrane performs better mechanical properties than the collagen film. Moreover, the modified film proves excellent biocompatibility for the proliferation of human corneal epithelial cells in vitro. This Col-CS film with good moisturizing properties can reduce the risk of xerophthalmia and is expected to increase the implant success rate in clinic patients with corneal defects.  相似文献   

    

Xiaoqiang Wang;Chao Song;Daqian Zhou;Yongliang Mei;Weiye Cai;Rui Chen;Jiale Lv;Houyin Shi;Zongchao Liu; 《JOR SPINE》2024,7(4):e70020

Intervertebral disc degeneration (IVDD) stands as a prevalent chronic orthopedic ailment, profoundly impacting patients' well-being due to incapacitating low back pain. Studies have highlighted a close correlation between IVDD and the programmed cell death of nucleus pulposus (NP) cells orchestrated by interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and caspase-3 (CASP3). Puerarin, renowned for its anti-inflammatory attributes and its influence on IL-1β and TNF-α, emerges as a promising candidate for IVDD treatment. However, the precise mechanism by which it regulates apoptosis via these pathways remains ambiguous. This investigation utilizes bioinformatics to unveil the molecular intricacies of puerarin-mediated apoptosis regulation in IVDD, substantiated by preliminary in vitro experiments. Analysis exposes aberrant expression of pivotal apoptosis-associated proteins (IL-1β, TNF-α, CASP3, CASP8, and BCL2) in IVDD patients, with network pharmacology indicating puerarin's potential efficacy in IVDD treatment by modulating apoptosis and cellular senescence pathways. Further experiments elucidate puerarin's capacity to stimulate NP cell proliferation while inhibiting apoptosis, potentially contributing to IVDD mitigation. Western blot and PCR outcomes reveal escalated expression of apoptosis-related proteins (IL-1β, TNF-α, and CASP3) in lipopolysaccharide-treated NPCs, ameliorated by puerarin intervention. Molecular docking simulations demonstrate favorable binding properties of puerarin with apoptotic proteins, while flow cytometry analysis indicates its ability to diminish NPC apoptosis. These discoveries imply that puerarin might alleviate NPC apoptosis by modulating key targets, thereby potentially ameliorating IVDD. In summary, this study unveils the intrinsic mechanism of puerarin in regulating NPC apoptosis to alleviate IVDD, underscoring its therapeutic promise.  相似文献   

    

Shixiong Wei;Yiyuan Zhang;Feixiang Luo;Kexing Duan;Mingqian Li;Guoyue Lv; 《Bioengineering & Translational Medicine》2024,9(4):e10671

Restoration of extensive tracheal damage remains a significant challenge in respiratory medicine, particularly in instances stemming from conditions like infection, congenital anomalies, or stenosis. The trachea, an essential element of the lower respiratory tract, constitutes a fibrocartilaginous tube spanning approximately 10–12 cm in length. It is characterized by 18 ± 2 tracheal cartilages distributed anterolaterally with the dynamic trachealis muscle located posteriorly. While tracheotomy is a common approach for patients with short-length defects, situations requiring replacement arise when the extent of lesion exceeds 1/2 of the length in adults (or 1/3 in children). Tissue engineering (TE) holds promise in developing biocompatible airway grafts for addressing challenges in tracheal regeneration. Despite the potential, the extensive clinical application of tissue-engineered tracheal substitutes encounters obstacles, including insufficient revascularization, inadequate re-epithelialization, suboptimal mechanical properties, and insufficient durability. These limitations have led to limited success in implementing tissue-engineered tracheal implants in clinical settings. This review provides a comprehensive exploration of historical attempts and lessons learned in the field of tracheal TE, contextualizing the clinical prerequisites and vital criteria for effective tracheal grafts. The manufacturing approaches employed in TE, along with the clinical application of both tissue-engineered and non-tissue-engineered approaches for tracheal reconstruction, are discussed in detail. By offering a holistic view on TE substitutes and their implications for the clinical management of long-segment tracheal lesions, this review aims to contribute to the understanding and advancement of strategies in this critical area of respiratory medicine.  相似文献