Dawei Yang

Harbin Medical University

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Fan Yang

Guizhou Provincial People's Hospital

Jian Wu

Southern Medical University

Yinan Zhou

Wuxi No.2 People's Hospital

Ai Okamura

Astellas Pharma (Japan)

Makoto Kodama

Tokyo Yamate Medical Center

Mingjie He

Chengdu University of Traditional Chinese Medicine

Biaoliang Wu

Affiliated Hospital of Youjiang Medical University for Nationalities

Yoshiaki Shiba

National Institute of Advanced Industrial Science and Technology

Kunzheng Wang

Second Affiliated Hospital of Xi'an Jiaotong University

Gui‐Bin Qian

Harbin Medical University

Cooperative Institutions

Harbin Medical University

Second Affiliated Hospital of Harbin Medical University

National Institute of Advanced Industrial Science and Technology

Nanjing Medical University

Central South University

Fudan University

Affiliated Hospital of Youjiang Medical University for Nationalities

Youjiang Medical College for Nationalities

Huazhong University of Science and Technology

Xiangya Hospital Central South University

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Ascorbic acid 2-phosphate enhances albumin mRNA expression and secretion of porcine hepatocytes

Materials Science and Engineering C (2004)

Dawei Yang Toshie Koyama Ai Okamura Yoshiaki Shiba Takayuki Akimoto

Serum Albumin

10.1016/j.msec.2003.12.015

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Citations (1)

Associations of Sex Hormone-binding Globulin with Bone Mineral Density Among US Adults, NHANES 2013–2016

International Journal of General Medicine (2021)

Fan Yang Dawei Yang Yinan Zhou Jian Wu

Background: Bone metabolism can be influenced by sex steroid hormones. However, the relationship between sex steroid hormones and bone mineral density (BMD) remains inconsistent. Our study explored existing evidence of the association between sex hormones, blood glucose and BMD. Methods: We conducted a cross-sectional study of 6434 participants aged 18– 80 years in the National Health and Nutrition Examination Survey (NHANES) 2013– 2016 to assess the association between SHBG and BMD. The multivariable linear regression models were performed to evaluate the associations between testosterone, estrogen, sex hormone-binding globulin (SHBG) and BMD. Results: On adjustment for traditional risk factors (age, BMI, ALB, ALK, ASP, calcium, cholesterol, potassium, sodium, total protein, uric acid), SHBG could be regarded as an independent predictor for BMD, while fasting blood glucose did not. SHBG levels were significant associated with BMD in the multivariate model; however, it will be a different effect between the genders. On comparative analysis, high level SHBG was predictive of lumbar BMD irrespective of other two sex steroid hormones. Conclusion: This study indicated that SHBG may improve the predictive value for bone loss in adults. Keywords: sex steroid hormones, SHBG, bone mineral density, NHANES

Sex steroid

10.2147/ijgm.s329992

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Citations (9)

RETRACTED ARTICLE: Inhibition of microRNA-495 suppresses chondrocyte apoptosis through activation of the NF-κB signaling pathway by regulating CCL4 in osteoarthritis

Gene Therapy (2019)

Dawei Yang Gui‐Bin Qian Ming‐Jiu Jiang Peng Wang Kunzheng Wang

10.1038/s41434-019-0068-5

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Citations (37)

Associations Among Microvascular Dysfunction, Fatty Acid Metabolism, and Diabetes

Cardiovascular Innovations and Applications (2023)

Jian Wu Youqi Zhang Liu Ji Suhong Zhao Yueqing Han

Diabetes mellitus is a chronic metabolic disorder characterized by elevated blood glucose levels resulting from impaired insulin secretion or insulin resistance. Diabetes poses a major global health concern, because of its increasing prevalence and substantial morbidity and mortality. This review explores the relationships between altered fatty acid metabolism and microcirculatory impairments in diabetes. Dysregulation of fatty acid metabolism in diabetes leads to changes in fatty acid profiles, abnormal lipid accumulation, and increased oxidative stress. These changes contribute to microvascular dysfunction through mechanisms such as endothelial dysfunction, impaired nitric oxide availability, inflammation, and oxidative damage. Understanding this intricate interplay is essential for identifying novel therapeutic strategies to alleviate vascular complications in diabetes. By targeting specific pathways involved in fatty acid metabolism and microvascular dysfunction, interventions can be developed to improve patient outcomes. This review is aimed at contributing to future research and the development of effective strategies for preventing and managing diabetes-associated microcirculatory impairments, to ultimately enhance the quality of life for people living with diabetes.

Endothelial Dysfunction

Fatty Acid Metabolism

10.15212/cvia.2023.0076

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Citations (3)

Pathogenic Cx31 is un/misfolded to cause skin abnormality via a Fos/JunB-mediated mechanism

Human Molecular Genetics (2015)

Chengyuan Tang Xiang Chen Jingwei Chi Dawei Yang Shu Liu

Mutations in connexin-31 (Cx31) are associated with multiple human diseases, including familial erythrokeratodermia variabilis (EKV). The pathogenic mechanism of EKV-associated Cx31 mutants remains largely elusive. Here, we show that EKV-pathogenic Cx31 mutants are un/misfolded and temperature sensitive. In Drosophila, expression of pathogenic Cx31, but not wild-type Cx31, causes depigmentation and degeneration of ommatidia that are rescued by expression of either dBip or dHsp70. Ectopic expression of Cx31 in mouse skin results in skin abnormalities resembling human EKV. The affected tissues show remarkable disrupted gap junction formation and significant upregulation of chaperones Bip and Hsp70 as well as AP-1 proteins c-Fos and JunB, in addition to molecular signatures of skin diseases. Consistently, c-Fos, JunB, Bip and Hsp70 are strikingly higher in keratinocytes of EKV patients than their matched control individuals. Furthermore, a druggable AP-1 inhibitory small molecule suppresses skin phenotype and pathological abnormalities of transgenic Cx31 mice. The study suggests that Cx31 mutant proteins are un/misfolded to cause EKV likely via an AP-1-mediated mechanism and identifies a small molecule with therapeutic potential of the disease.

Ectopic expression

JUNB

10.1093/hmg/ddv317

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Citations (9)

Effect of Aluminum Exposure on Glucose Metabolism and Its Mechanism in Rats

Biological Trace Element Research (2018)

Xi Wei Hua Wei Dawei Yang Li Dong Xianli Yang

GLUT4

Carbohydrate Metabolism

Intraperitoneal injection

Alloxan

Homeostasis

10.1007/s12011-018-1318-x

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Citations (19)

Exercise may not just be good for sleep; It can also help lower cardiovascular event risk

Current Problems in Cardiology (2023)

Jianjun Wu Dawei Yang Fan Yang

Sleep

Cardiovascular Health

10.1016/j.cpcardiol.2023.102166

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Citations (1)

Hydrogen sulfide inhibits endoplasmic reticulum stress through the GRP78/mTOR pathway in rat chondrocytes subjected to oxidative stress

International Journal of Molecular Medicine (2021)

Jian Wu Fan Yang Xin Zhang Guanghua Chen Jilong Zou

The activation of oxidative stress is a primary cause of chondrocyte apoptosis in osteoarthritis (OA). The 78‑kDa glucose‑regulated protein (GRP78)/mammalian target of rapamycin (mTOR) signaling pathway has been demonstrated to be linked with the endoplasmic reticulum (ER) and autophagy. Hydrogen sulfide (H₂S) has been reported to exert antioxidant effects. The present study investigated oxidative stress levels via 2',7'‑dichlorofluorescin diacetate and MitoSOX staining, apoptosis rates via flow cytometry and the expression levels of ER stress‑related proteins in GYY4137 (donor of H₂S)‑treated chondrocytes (CHs). CHs were isolated from the bilateral hip joints of male rats to examine mitochondrial permeability transition pore opening‑ and mTOR signaling pathway‑related proteins. The results demonstrated that tert‑Butyl hydroperoxide (TBHP) increased CH apoptosis, and treatment with GYY4137 ameliorated TBHP‑mediated the generation of ROS and CH apoptosis. Moreover, TBHP‑treated CHs displayed elevated ER stress sensor expression levels and apoptotic rates; however, the TBHP‑induced protein expression levels were decreased following GYY4137 treatment. In the present study, treatment with either GYY4137 or transfection with GRP78 siRNA both suppressed the activation of p‑P70S6k and p‑mTOR. H₂S played an important role in regulating ER stress in TBHP‑stimulated CHs. GYY4137 promoted autophagy, which was accompanied by the inhibition of ER stress. On the whole, the present study demonstrates that TBHP‑induced oxidative stress stimulates ER interactions and CH apoptosis, which are suppressed by exogenous H₂S via modulating the GRP78/mTOR signaling pathway.

10.3892/ijmm.2021.4867

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Citations (13)

Expression of Human D-beta-Aspartate in Lens-Derived Cell Line

Viva origino (2001)

Dawei Yang Noriko Fujii Yoshiko Tanaka

BETA (programming language)

Line (geometry)

Source

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Effects of aluminum exposure on insulin secretion and insulin signaling pathway in rats

Trace Elements and Electrolytes (2019)

Mingjie He Xi Wei Dawei Yang Biaoliang Wu

10.5414/tex01601

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Citations (0)