Despite the status quo, the factors that precipitate the development and progression of DKD remain to be fully elucidated. The onset of clinically overt DKD is defined as persistent proteinuria and is most closely associated with podocytopathies that results from damage to the glomerular filtration barrier at the level of the highly differentiated glomerular podocyte cells. As one of the most frequent complications of DM, diabetic kidney disease (DKD) defined as a syndrome, is the most common metabolic disease in the world that is the leading cause of end-stage renal disease (ESRD) comprising about 40% of patients with chronic kidney disease (CKD). The incidence and prevalence of diabetes mellitus (DM) have grown significantly throughout the world due to the overall increase in type 2 diabetes (T2D). Keywords: Klotho, diabetes, mitochondrial dysfunction (MtD), podocyte injury, DNA damage Introduction Therefore, we came to a conclusion that Klotho deficiency may promote diabetes-induced podocytic MtD and aggravate 8-OHdG-induced DNA damage by affecting OOG1. Finally, we demonstrated Klotho deficiency may promote MtD to promote 8-OHdG-induced podocyte injury. Then, we further confirmed that Klotho deficiency could significantly aggravate DNA damage by increasing 8-OHdG and reducing OGG1. First, we found that the absence of Klotho aggravated diabetic phenotypes indicated by podocyte injury accompanied by elevated urea albumin creatinine ratio (UACR), creatinine and urea nitrogen. Here, we investigated the influence of Klotho deficiency on high glucose (HG)-induced DNA damage in vivo and in vitro. However, research on how mitochondrial dysfunction (MtD) ultimately causes DNA damage is poor. The occurrence and development of DN could be partly attributed to the reactive oxygen species (ROS) generated by mitochondria. File import instruction Abstractĭiabetic nephropathy (DN) is a progressive disease, the main pathogeny of which is podocyte injury inducing glomerular filtration barrier and proteinuria. Select the file that you have just downloaded and select import option Reference Manager (RIS).
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Klotho deficiency aggravates diabetes-induced podocyte injury due to DNA damage caused by mitochondrial dysfunction. MoreĬhen Z, Zhou Q, Liu C, Zeng Y, Yuan S. Universi ty-Town Clinic, 958 hospital of PLA Army, Chongqing, 400020, People's Republic of China. Department of orthopedics, Chongqing general hospital, University of Chinese Academy of Sciences, Chongqing, 400014, China. ✉ Corresponding authors: Yiping Zeng, M.D., Ph.D. Department of orthopedics, Chongqing general hospital, University of Chinese Academy of Sciences, Chongqing, 400014, People's Republic of China. Center of Laboratory Medicine, Chongqing Prevention and Treatment Center for Occupational Disease, Chongqing, 400060, People's Republic of China.Ĥ. School of Military Preventive Medicine, Army Military Medical University, Chongqing, 400020, People's Republic of China.ģ. University-Town Clinic, 958 hospital of PLA Army, Chongqing, 400020, People's Republic of China.Ģ. Zhi Chen 1, Qing Zhou 2, Cong Liu 3, Yiping Zeng 4, Shaolong Yuan 1ġ. Research Paper Klotho deficiency aggravates diabetes-induced podocyte injury due to DNA damage caused by mitochondrial dysfunction
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