Article
Biochemistry & Molecular Biology
Ziyan Lin, Ai Chen, Hongwang Cui, Ruihua Shang, Tian Su, Xiaoyan Li, Kekun Wang, Jing Yang, Keli Gao, Jie Lv, Jie Shen, Shanzhi Wang, Yonghui Qi, Minghao Guo, Yongjun Zhu
Summary: This study identified the occurrence of renal tubular epithelial cell necroptosis in CKD patients, especially in stages 2 and 3a CKD. Renal tubular epithelial cell necroptosis mediates renal tubulointerstitial fibrosis in patients with chronic kidney disease, which is related to the TGF-beta 1/Smad3 signaling pathway.
Review
Cell Biology
Shan Jiang, Hua Su
Summary: Diabetic kidney disease (DKD) is a major cause of end-stage renal disease and poses a significant economic burden globally. Understanding the complex pathophysiology of DKD is of utmost importance. While the cellular crosstalk between podocytes and endothelial cells in DKD is relatively well known, little is understood about the crosstalk between mesangial cells (MCs) and renal tubular epithelial cells (TECs). The recent recognition of the significance of MCs and TECs in DKD highlights the need for a comprehensive understanding of their cellular communication. Insights into the intricate mechanisms underlying DKD pathophysiology would greatly benefit early detection, treatment, and prognosis.
CELL COMMUNICATION AND SIGNALING
(2023)
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
Microbiology
Han Huang, Rui Ding, Zongyan Chen, Zewen Yi, Hongyu Wang, Yingjun Lv, Endong Bao
Summary: GNAstV infection in goslings leads to pathological changes in kidney tissue, including autophagy in renal epithelial cells, destruction of brush border and intercellular junctions, damage to podocytes, and increased fibrosis.
VETERINARY MICROBIOLOGY
(2021)
Review
Physiology
Peipei Wang, Jing Ouyang, Zhanjun Jia, Aihua Zhang, Yunwen Yang
Summary: The prevalence of renal diseases is increasing globally, yet the pathogenesis and effective treatments are still unclear. DNA damage and the related DNA damage response have been identified as common factors in acute kidney injury (AKI) and chronic kidney disease (CKD). Reactive oxygen species induced DNA damage is a common type involved in the development of these conditions. Recent developments in the field of DNA damage have provided insights into the role of DNA damage and DNA damage response in renal tubular epithelial cell injury. Focusing on DNA damage and DNA damage response may offer valuable diagnostic biomarkers and treatment strategies for renal diseases.
FRONTIERS IN PHYSIOLOGY
(2023)
Article
Cell Biology
Yan Jun Li, Jin Ma, Yik Wen Loh, Steven J. Chadban, Huiling Wu
Summary: The aim of this study was to investigate the impact of short-chain fatty acids on cellular pathways involved in the development of diabetic nephropathy. Short-chain fatty acids were found to provide protection against diabetic nephropathy in mice and exert anti-inflammatory and anti-fibrotic effects through direct effects on kidney cells. GPR43 and GPR109A were identified as critical factors in short-chain fatty acid mediated reno-protection and could be potential therapeutic targets for diabetic nephropathy.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Lini Jin, Binfeng Yu, Guangjun Liu, Wanyun Nie, Junni Wang, Jianghua Chen, Liang Xiao, Hongguang Xia, Fei Han, Yi Yang
Summary: Activation of mitophagy improves mitochondrial health, reduces TGF-beta 1/Smad signaling, alleviates TEC injuries, and decreases inflammatory infiltration in the kidneys.
Article
Cell Biology
Ying Yang, Chensheng Li, Xia Gu, Junhui Zhen, Suwei Zhu, Tingting Lv, Qiang Wan, Yi Liu
Summary: The study demonstrated that ING2 plays a crucial role in modulating mitochondrial respiration of TECs by regulating mtDNA transcription and the abundance of respiratory chain components. ING2 also showed to be involved in the ubiquitination of mitochondrial transcription factor MRPL12, affecting TEC mitochondrial function. Additionally, ING2-mediated modulation on mtDNA transcription and mitochondrial respiration were found to be associated with TEC injuries induced by serum deprivation.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Cell Biology
Ying Yang, Chensheng Li, Xia Gu, Junhui Zhen, Suwei Zhu, Tingting Lv, Qiang Wan, Yi Liu
Summary: ING2 plays a crucial role in regulating mitochondrial respiration in tubular epithelial cells, potentially maintaining mitochondrial homeostasis by modulating mtDNA transcription and respiratory chain components. Additionally, ING2 regulates the ubiquitination of a mitochondrial transcription factor MRPL12, and has a protective effect on tubular epithelial cells against acute ischemic injury.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Medicine, General & Internal
Yinghong Liu, Mingyue He, Hao Xiong, Fang Yuan
Summary: This study found that high glucose can increase the expression of inflammation-related proteins NLRP3 and GSDMD in kidney tissues of DKD patients, and induce pyroptosis in HK-2 cells. There is a correlation between glucose concentration and pyroptosis, which is significant for the treatment of DKD patients.
FRONTIERS IN MEDICINE
(2022)
Article
Biochemistry & Molecular Biology
Xingzhao Ji, Xiaoli Yang, Xia Gu, Lingju Chu, Shengnan Sun, Jian Sun, Peng Song, Qian Mu, Ying Wang, Xiaoming Sun, Dun Su, Tong Su, Shaoshuai Hou, Yao Lu, Chen Ma, Mingqiang Liu, Tianyi Zhang, Weiying Zhang, Yi Liu, Qiang Wan
Summary: Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease and mortality in diabetic patients. This study reveals that mitochondrial ribosomal protein L12 (MRPL12) plays a crucial role in DKD by affecting mitochondrial function. Cullin3 (CUL3), an E3 ubiquitin ligase, has been identified to mediate the ubiquitination of MRPL12, leading to mitochondrial biosynthesis dysfunction. The findings suggest a potential therapeutic strategy for DKD by targeting the CUL3-MRPL12 pathway.
Article
Biochemistry & Molecular Biology
Yao Zhang, Jianjian Zhang, Dengyuan Feng, Hai Zhou, Zeping Gui, Ming Zheng, Zhou Hang, Zijie Wang, Zengjun Wang, Min Gu, Ruoyun Tan
Summary: This study revealed that ferroptosis of renal tubular epithelial cells (RTECs) may contribute to renal tubular injury in chronic renal allograft dysfunction (CAD). TNF-alpha induced ferroptosis by inhibiting GPX4 transcription through upregulating IRF1 in RTECs. Ferroptotic RTECs might secrete profibrotic factors to activate neighboring fibroblasts or induce EMT in adjacent RTECs.
FREE RADICAL BIOLOGY AND MEDICINE
(2022)
Article
Cell Biology
Huzi Xu, Meng Wang, Yinzheng Li, Mengxia Shi, Zheng Wang, Chujin Cao, Yu Hong, Bin Hu, Han Zhu, Zhi Zhao, Xiaoxin Chu, Fan Zhu, Xuan Deng, Jianliang Wu, Fenfei Zhao, Jing Guo, Yuxi Wang, Guangchang Pei, Fengming Zhu, Xiaoyan Wang, Juan Yang, Ying Yao, Rui Zeng
Summary: This study explores the role of connexin 43 (Cx43) in renal fibrosis and the release of ATP from injured renal tubular epithelial cells (TECs). The findings demonstrate that Cx43 is upregulated in TECs and its depletion reduces inflammation and fibrosis in obstructive nephropathy. The release of ATP induces macrophage pyroptosis, leading to the activation of fibroblasts and acceleration of renal fibrosis.
CELL DEATH & DISEASE
(2022)
Review
Endocrinology & Metabolism
Jun-Qing Zhang, Ying-Ying Li, Xue-Yan Zhang, Zeng-Hui Tian, Cheng Liu, Shi-Tao Wang, Fa-Rong Zhang
Summary: Renal fibrosis is a common pathological manifestation of chronic kidney diseases and a major cause of end-stage renal disease, but its pathogenesis remains unclear. Renal tubular epithelial cell senescence has been found to accelerate the progression of renal fibrosis. Oxidative stress, telomere attrition, and DNA damage are the major causes of renal tubular epithelial cell senescence. Interventions and therapeutic strategies targeting cellular senescence, such as calorie restriction, exercise, Klotho, senolytics, and senostatics, show potential for the treatment of renal fibrosis.
FRONTIERS IN ENDOCRINOLOGY
(2023)
Article
Medicine, Research & Experimental
Shuiqin Gong, Aihong Zhang, Mengying Yao, Wang Xin, Xu Guan, Shaozong Qin, Yong Liu, Jiachuan Xiong, Ke Yang, Li Xiong, Ting He, Yinghui Huang, Jinghong Zhao
Summary: Ischemic-reperfusion injury (IRI) is a major factor in acute kidney injury (AKI) that leads to hypoxic injury of renal tubular epithelial cells (RTECs). The upregulation of repressor element 1-silencing transcription factor (REST) in AKI patients, mice, and RTECs is positively correlated with the severity of kidney injury. Knockout of Rest in renal tubules significantly alleviates AKI and its progression to chronic kidney disease (CKD). These findings highlight the involvement of REST in the transition from AKI to CKD and reveal its ferroptosis-inducing effect, suggesting it as a potential therapeutic target for AKI and CKD.
