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23 results on '"Zhang, Jia Xiu"'

10. Deficiency of thiosulfate sulfurtransferase mediates the dysfunction of renal tubular mitochondrial fatty acid oxidation in diabetic kidney disease

Author

Zhang, Jia Xiu, Chen, Pei Pei, Li, Xue Qi, Li, Liang, Wu, Qin Yi, Wang, Gui Hua, Ruan, Xiong Zhong, and Ma, Kun Ling

Abstract

One of the main characteristics of diabetic kidney disease (DKD) is abnormal renal tubular fatty acid metabolism, especially defective fatty acid oxidation (FAO), accelerating tubular injury and tubulointerstitial fibrosis. Thiosulfate sulfurtransferase (TST), a mitochondrial enzyme essential for sulfur transfer, is reduced in metabolic diseases like diabetes and obesity. However, the potential role of TST in regulating fatty acid metabolic abnormalities in DKD remains unclear. Here, our data revealed decreased TST expression in the renal cortex of DKD patients. TST deficiency exacerbated tubular impairment in both diabetic and renal fibrosis mouse models, while sodium thiosulfate treatment or TST overexpression mitigated renal tubular injury with high-glucose exposure. TST downregulation mediated the decrease in S-sulfhydration of very long-chain specific acyl-CoA dehydrogenase, resulting in mitochondrial FAO dysfunction. This sequence of events exacerbates the progression of tubulointerstitial injury in DKD. Together, our findings demonstrate TST as a regulator of renal tubular injury in DKD.

Published
2024
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13. Deposition of platelet-derived microparticles in podocytes contributes to diabetic nephropathy

Author

Huang, Si Jia, primary, Zhang, Yang, additional, Wang, Gui Hua, additional, Lu, Jian, additional, Chen, Pei Pei, additional, Zhang, Jia Xiu, additional, Li, Xue Qi, additional, Yuan, Ben Yin, additional, Liu, Xiao Qi, additional, Jiang, Ting Ting, additional, Wang, Meng Ying, additional, Liu, Wen Tao, additional, Ruan, Xiong Zhong, additional, Liu, Bi Cheng, additional, and Ma, Kun Ling, additional

Published
2022
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14. GPR43 activation-mediated lipotoxicity contributes to podocyte injury in diabetic nephropathy by modulating the ERK/EGR1 pathway

Author

Lu, Jian, primary, Chen, Pei Pei, additional, Zhang, Jia Xiu, additional, Li, Xue Qi, additional, Wang, Gui Hua, additional, Yuan, Ben Yin, additional, Huang, Si Jia, additional, Liu, Xiao Qi, additional, Jiang, Ting Ting, additional, Wang, Meng Ying, additional, Liu, Wen Tao, additional, Ruan, Xiong Zhong, additional, Liu, Bi Cheng, additional, and Ma, Kun Ling, additional

Published
2022
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17. GPR43 deficiency protects against podocyte insulin resistance in diabetic nephropathy through the restoration of AMPKα activity

Author

Lu, Jian, primary, Chen, Pei Pei, additional, Zhang, Jia Xiu, additional, Li, Xue Qi, additional, Wang, Gui Hua, additional, Yuan, Ben Yin, additional, Huang, Si Jia, additional, Liu, Xiao Qi, additional, Jiang, Ting Ting, additional, Wang, Meng Ying, additional, Liu, Wen Tao, additional, Ruan, Xiong Zhong, additional, Liu, Bi Cheng, additional, and Ma, Kun Ling, additional

Published
2021
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22. Influence of Iodine Deficiency on Human Fetal Thyroid Gland and Brain

Author

Zhang Jia-Xiu, Chen Bin-Zhon, Shi Zhon-Fu, Zhuang Zhong-Jie, Tan Yu-Bin, and Liu Jia-Liu

Subjects
Fetus, medicine.medical_specialty, Goiter, business.industry, Thyroid, Aborted Fetus, chemistry.chemical_element, medicine.disease, Iodine, Iodine deficiency, Iodised salt, Endocrinology, medicine.anatomical_structure, chemistry, Internal medicine, embryonic structures, medicine, business, Cretinism, reproductive and urinary physiology
Abstract

In order to evaluate the influence of prenatal iodine deficiency on the thyroid gland and brain in man, we studied therapeutically aborted fetuses collected from a severely iodine deficient endemic goiter and cretinism area before and after 5 year iodized salt utilization. Fetuses from a non-endemic area served as the normal controls1,2,3.

Published
1989

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