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    Home > Active Ingredient News > Endocrine System > Redox biology: Ma Chunhong/Professor Yang Xiangdong's team made new progress in the field of diabetic nephropathy and autophagy regulation

    Redox biology: Ma Chunhong/Professor Yang Xiangdong's team made new progress in the field of diabetic nephropathy and autophagy regulation

    • Last Update: 2022-03-04
    • Source: Internet
    • Author: User
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    Recently, the team of Professor Ma Chunhong from the School of Basic Medicine and Professor Yang Xiangdong from Qilu Hospital published a collaborative research titled "Upregulation of TIPE1 in tubular epithelial cell aggravates diabetic nephropathy by disrupting PHB2 mediated mitophagy" in the journal Redox biology (District 1, Chinese Academy of Sciences, IF=11.
    799 ).
    results .
    Liu Lei, a doctoral student at the School of Clinical Medicine, is the first author, Professor Liang Xiaohong of Shandong University and Professor Yang Xiangdong of the Department of Nephrology of Qilu Hospital are the co-corresponding authors, and Shandong University is the first author and the only corresponding author .

    Recently, the team of Professor Ma Chunhong from the School of Basic Medicine and Professor Yang Xiangdong from Qilu Hospital published a collaborative research titled "Upregulation of TIPE1 in tubular epithelial cell aggravates diabetic nephropathy by disrupting PHB2 mediated mitophagy" in the journal Redox biology (District 1, Chinese Academy of Sciences, IF=11.


    799 ).
    results .


    According to the statistics of the World Diabetes Association , the incidence of diabetes is increasing year by year, and by 2035 , there will be approximately 592 million diabetic patients
    .


    Diabetic nephropathy is one of the important complications of diabetes with complex pathogenesis, among which the damage of renal tubular epithelial cells and fibrosis are the main reasons for the decline of renal function


    According to the statistics of the World Diabetes Association , the incidence of diabetes is increasing year by year, and by 2035 , there will be about 592 million diabetic patients .
    Diabetic nephropathy is one of the important complications of diabetes with complex pathogenesis, among which the damage of renal tubular epithelial cells and fibrosis are the main reasons for the decline of renal function .
    This study revealed for the first time that tumor necrosis factor alpha -inducible protein 8 -like molecule 1 (TIPE1) increased expression under high glucose stimulation and resulted in impaired mitochondrial function of renal tubular epithelial cells, thereby promoting the progression of diabetic nephropathy .


    Professor Ma Chunhong's team and Professor Yang Xiangdong's team are mainly engaged in the research on immune microenvironment and metabolic diseases.
    In the previous collaborative research, it was found that the immune regulatory molecule immune Tim3 activates the NF-κB signaling pathway in macrophages and aggravates the progression of diabetic nephropathy .
    Relevant research results have been published in important international journals such as J Exp Med , GUT , Cell Mol Immunol , J HEPATOL , CANCER RES , Molecular Metabolism , Cell Death and Differentiation .
    The above research was supported by the National Natural Science Foundation of China Key Project, the National Natural Science Foundation of China General Project, and the National Key Research and Development Program .
    Natural Science Foundation

    Original link:

    Original link:

    Upregulation of TIPE1 in tubular epithelial cell aggravates diabetic nephropathy by disrupting PHB2 mediated mitophagy .


    Redox biology.
    2022.
    https://doi.


    Upregulation of TIPE1 in tubular epithelial cell aggravates diabetic nephropathy by disrupting PHB2 mediated mitophagy .
    Redox biology.
    2022.
    https://doi.
    org/10.
    1016/j.
    redox.
    2022.
    102260 Upregulation of TIPE1 in tubular epithelial cell aggravates diabetic nephropathy by disrupting PHB2 mediated mitophagy leave a message here
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