Article
Cell Biology
Aimei Li, Bin Yi, Hailong Han, Shikun Yang, Zhaoxin Hu, Li Zheng, Jianwen Wang, Qin Liao, Hao Zhang
Summary: The study demonstrates that VD-VDR can restore defective autophagy in the kidneys of STZ-induced diabetic mice through activation of the Ca2+-CAMKK2-AMPK pathway in renal tubular epithelial cells.
Article
Biochemistry & Molecular Biology
Li Zhang, Chong-sen Zang, Bin Chen, Yu Wang, Shuai Xue, Mei-yan Wu
Summary: Diabetic nephropathy (DN) is a major complication of diabetes and the leading cause of end-stage renal disease worldwide. Renalase (RNLS) is an amine oxidase produced by renal tubular epithelial cells and is closely related to renal tubular injury in kidney diseases. This study evaluated the changes in tubular RNLS expression in DN and its correlation with renal tubular injury.
Article
Genetics & Heredity
Jiayi Wan, Mingyang Hu, Ziming Jiang, Dongwei Liu, Shaokang Pan, Sijie Zhou, Zhangsuo Liu
Summary: This study analyzed the acetylation levels of proteins in mouse renal tubular epithelial cells cultured in vitro under high glucose conditions. The majority of acetylated proteins were found in mitochondria, nucleus, and cytoplasm, associated with oxidative phosphorylation and metabolic pathways. This comprehensive analysis provides novel insights into the role of lysine acetylation in tubular epithelial cells and diabetic nephropathy.
FRONTIERS IN GENETICS
(2021)
Article
Cell Biology
Yanjuan Hou, Qian Wang, Baosheng Han, Yiliang Chen, Xi Qiao, Lihua Wang
Summary: In diabetic nephropathy, CD36 mediates ROS production that enhances NLRP3 inflammasome activation, leading to IL-1 beta secretion and cell apoptosis. Inhibition of CD36 protects mice from tubulointerstitial inflammation and tubular epithelial cell apoptosis.
CELL DEATH & DISEASE
(2021)
Article
Cell Biology
DongWei Liu, FengXun Liu, ZhengYong Li, ShaoKang Pan, JunWei Xie, ZiHao Zhao, ZhenJie Liu, JiaHui Zhang, ZhangSuo Liu
Summary: This study found that miR-483-5p is decreased in kidney tissues of diabetic mice and in tubular epithelial cells stimulated with high glucose, but increased in exosomes derived from diabetic mouse kidney tissues. miR-483-5p inhibits fibrosis-related gene expressions by binding to TIMP2 and MAPK1, thus alleviating the progression of DN-induced renal interstitial fibrosis.
CELL DEATH & DISEASE
(2021)
Article
Biochemistry & Molecular Biology
Theodoros Eleftheriadis, Georgios Pissas, Georgios Filippidis, Maria Efthymiadi, Vassilios Liakopoulos, Ioannis Stefanidis
Summary: Gliflozins, such as dapagliflozin, can inhibit cell senescence pathways and prevent renal tubular epithelial cell (RPTEC) senescence. High glucose induces oxidative stress and leads to a senescence-associated secretory phenotype. Dapagliflozin reduces glucose consumption and inhibits related pathways, effectively preventing cell senescence. Investigating the effects of gliflozins on cell senescence has potential significance for the treatment of diabetic nephropathy.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Endocrinology & Metabolism
Liping Mai, Guodong He, Jing Chen, Jiening Zhu, Shaoxian Chen, Hui Yang, Mengzhen Zhang, Xinghua Hou, Miaola Ke, Xiaohong Li
Summary: The study found that PFN1 is significantly upregulated in diabetic nephropathy and is associated with cell apoptosis and senescence. Overexpression of PFN1 promotes apoptosis and inhibits proliferation in high glucose-treated HK-2 cells, while knockdown of PFN1 has the opposite effects. Furthermore, PFN1 is correlated with the inactivation of the Hedgehog signaling pathway in high glucose-treated HK-2 cells.
DIABETES METABOLIC SYNDROME AND OBESITY
(2023)
Article
Biochemistry & Molecular Biology
Shuguang Yuan, Youliang Wang, Zheng Li, Xiaojun Chen, Panai Song, Anqun Chen, Zhong Qu, Si Wen, Hong Liu, Xuejing Zhu
Summary: The study revealed that TLR4 may exacerbate tubular injury and fibrosis in T2DKD through the GSDMD-mediated pyroptosis pathway. Activation of GSDMD can inhibit apoptosis and activate pyroptosis, which may involve a potential switch mechanism between TLR4-mediated pyroptosis and apoptosis.
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
(2022)
Article
Immunology
Sean E. DeWolf, Sashi G. Kasimsetty, Alana A. Hawkes, Lisa M. Stocks, Sunil M. Kurian, Dianne B. McKay
Summary: This study demonstrates for the first time that endogenous DAMPs released from injured RTECs directly activate PRR signaling in healthy RTECs. These findings provide new insights for the treatment of renal IRI.
Article
Cell Biology
Chen Yang, Xiao-Cui Chen, Zhi-Hang Li, Hong-Luan Wu, Kai-Peng Jing, Xiao-Ru Huang, Lin Ye, Biao Wei, Hui-Yao Lan, Hua-Feng Liu
Summary: SMAD3 induces lysosome depletion via inhibition of TFEB-dependent lysosome biogenesis, which may play a crucial role in the dysregulation of autophagy in diabetic nephropathy.
Article
Cell Biology
Yanan Gong, Yanna Dou, Luyao Wang, Xiaoyang Wang, Zhanzheng Zhao
Summary: This study found that EP300 gene is closely related to the development and progression of diabetic nephropathy (DN), and can promote the fibrotic processes of renal tubular epithelial cells by increasing the expression of HIF2 alpha.
CELLULAR SIGNALLING
(2022)
Article
Environmental Sciences
Chin-Yi Lin, Yu-Cheng Lin, Catherine Reena Paul, Dennis Jine-Yuan Hsieh, Cecilia Hsuan Day, Ray-Jade Chen, Chia-Hua Kuo, Tsung-Jung Ho, Marthandam Asokan Shibu, Chin-Hu Lai, Tzu-Ching Shih, Wei-Wen Kuo, Chih-Yang Huang
Summary: Diabetic nephropathy is a serious complication in diabetic patients, which is caused by hyperglycemia-associated advanced glycation end-products. This study found that isoliquiritigenin can effectively inhibit renal tubular fibrosis induced by these glycation end-products.
ENVIRONMENTAL TOXICOLOGY
(2022)
Article
Cell Biology
Zhaoxia Xu, Keqi Jia, Hui Wang, Feng Gao, Song Zhao, Fan Li, Jun Hao
Summary: HDAC5 plays a role in regulating EMT in HK2 cells by modulating TGF-beta 1, which can be influenced by the PI3K/Akt signaling pathway. METTL14, an m6A modification-associated enzyme, affects PI3K/Akt pathway through PTEN, leading to HDAC5-mediated EMT of renal tubular cells in diabetic kidney disease. Treatment with HDAC inhibitor TSA can alleviate extracellular matrix accumulation in kidneys of diabetic mice by downregulating HDAC5, TGF-beta 1, and alpha -SMA expression.
CELL DEATH & DISEASE
(2021)
Article
Biology
Chuanqiang Zhou, Min Wu, Gaolun Liu, Li Zhou
Summary: The aim of this study was to investigate the role of ferroptosis in diabetic nephropathy (DN) and the mechanism of its regulatory genes. The results showed that heterochromatin protein 1 is an abnormally elevated gene related to DN and is further elevated by ferroptosis activators. Inhibition of HP1 significantly inhibited ferroptosis but promoted cell viability.
OPEN LIFE SCIENCES
(2023)
Article
Biochemistry & Molecular Biology
Theodoros Eleftheriadis, Georgios Pissas, Spyridon Golfinopoulos, Maria Efthymiadi, Christina Poulianiti, Maria Anna Polyzou Konsta, Vassilios Liakopoulos, Ioannis Stefanidis
Summary: This study evaluated the response of renal proximal tubular epithelial cells (RPTECs) to high albumin concentration, focusing on the unfolded protein response (UPR) and DNA damage response (DDR). The results showed that albumin led to reactive oxygen species (ROS) overproduction and protein modification, which activated both UPR and DDR. This resulted in cellular apoptosis, senescence, and epithelial-to-mesenchymal transition (EMT). While agents against endoplasmic reticulum stress (ERS) only partially alleviated the harmful effects, inhibiting ROS upregulation prevented both UPR and DDR. Therefore, suppressing ROS overproduction may be more effective in mitigating the deleterious effects of albumin overload.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)