Article
Biochemistry & Molecular Biology
Qianqian Yang, Shuqing Yang, Yuehong Liang, Qi Sun, Yi Fang, Lei Jiang, Ping Wen, Junwei Yang
Summary: This study aimed to investigate whether UCP2 promotes autophagy in podocytes and explore the regulation mechanism of UCP2. The results showed that UCP2 expression increased in podocytes under diabetic conditions, and it protected against podocyte injury. However, UCP2 deficiency impaired autophagy and exacerbated podocyte injury and proteinuria in diabetic nephropathy.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
(2023)
Article
Biotechnology & Applied Microbiology
Hanying Ding, Jinxiang Li, Yang Li, Minliang Yang, Sheng Nie, Miaomiao Zhou, Zhanmei Zhou, Xiaobing Yang, Youhua Liu, Fan Fan Hou
Summary: This study identified miR-10a/b as negative regulators of NLRP3 inflammasome in diabetic kidney disease, preventing renal inflammation and reducing albuminuria. Targeting miR-10a/b could be a novel intervention strategy for inhibiting kidney inflammation in DKD.
Review
Nutrition & Dietetics
Ran Nakamichi, Kaori Hayashi, Hiroshi Itoh
Summary: Podocytes are highly differentiated cells that cover the outside of glomerular capillaries, and damage to podocytes leads to proteinuria and glomerulosclerosis. Diabetes is a main cause of CKD, making it crucial to understand its effects on podocytes for preventing CKD progression.
Review
Medicine, Research & Experimental
Xiandeng Li, Ying Zhang, Xiaodong Xing, Mi Li, Yan Liu, Ajing Xu, Jian Zhang
Summary: Diabetic nephropathy is a severe complication of diabetes mellitus, and understanding the underlying mechanisms of podocyte injury is key to developing effective therapeutic interventions. This review summarizes the factors contributing to podocyte injury in DN, including lipotoxicity, hemodynamic abnormalities, oxidative stress, mitochondrial dysfunction, and impaired autophagy. The findings presented in this review provide potential therapeutic targets and strategies for the management of DN associated with podocyte injury.
BIOMEDICINE & PHARMACOTHERAPY
(2023)
Article
Pharmacology & Pharmacy
Xi-Zhi Li, Hong Jiang, Liu Xu, Yi-Qi Liu, Jia-Wei Tang, Jia-Sen Shi, Xiu-Juan Yu, Xue Wang, Lei Du, Qian Lu, Cheng-Lin Li, Yao-Wu Liu, Xiao-Xing Yin
Summary: Sarsasapogenin (Sar) prevents podocyte injury in diabetic rats through targeting the GSK3 beta signaling pathway and restoring podocyte autophagy, thus ameliorating experimental DN.
BIOCHEMICAL PHARMACOLOGY
(2021)
Article
Plant Sciences
Zhi Wang, Qiao Wu, Hongzhan Wang, Yang Gao, Kexin Nie, Yueheng Tang, Hao Su, Meilin Hu, Jing Gong, Ke Fang, Hui Dong
Summary: This study found that diosgenin could protect against podocyte injury in the early phase of diabetic nephropathy by regulating SIRT6, and this effect was confirmed in animal experiments and cell experiments.
Article
Biochemistry & Molecular Biology
Makoto Tagaya, Shinji Kume, Mako Yasuda-Yamahara, Shogo Kuwagata, Kosuke Yamahara, Naoko Takeda, Yuki Tanaka, Masami Chin-Kanasaki, Yuki Nakae, Hideki Yokoi, Masashi Mukoyama, Naotada Ishihara, Masatoshi Nomura, Shin-ichi Araki, Hiroshi Maegawa
Summary: The mechanisms underlying the progression from endothelial damage to podocyte damage in diabetic kidney disease (DKD) and the development of massive proteinuria are investigated. Dynamin-related protein 1 (Drp1)-mediated regulation of mitochondrial fission in podocytes plays a role in the pathogenesis of proteinuria in DKD. Inhibition of mitochondrial fission in podocytes may represent a new therapeutic strategy for massive proteinuria in DKD.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
(2022)
Article
Pharmacology & Pharmacy
Wenmin Dong, Chenglin Jia, Ji Li, Yi Zhou, Yun Luo, Jibo Liu, Zhiguo Zhao, Jiaqi Zhang, Shan Lin, Ying Chen
Summary: This study finds that fisetin can alleviate high glucose-induced podocyte injury and STZ-induced DN by restoring autophagy-mediated CDKN1B/P70S6K pathway and inhibiting NLRP3 inflammasome.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Luna Jimenez-Castilla, Gema Marin-Royo, Macarena Orejudo, Lucas Opazo-Rios, Teresa Caro-Ordieres, Ines Artaiz, Tatiana Suarez-Cortes, Arturo Zazpe, Gonzalo Hernandez, Carmen Gomez-Guerrero, Jesus Egido
Summary: The synthetic flavonoid hidrosmin has shown protective effects against diabetic nephropathy by reducing inflammation, oxidative stress, and senescence pathways. It may have potential as an adjuvant therapy for chronic complications of diabetes mellitus. Additionally, hidrosmin demonstrated no cytotoxicity at effective concentrations, making it a promising treatment option.
Review
Immunology
Xiaokang Wang, Jingqian Zhao, Yuanqing Li, Jiaoyu Rao, Gengrui Xu
Summary: Proteinuria and nephrotic syndrome are symptoms of kidney diseases caused by direct or indirect damage to podocytes. Inflammation plays a crucial role in the development and progression of diabetic nephropathy, the leading cause of end-stage renal disease worldwide. The impact of podocyte damage on metabolic and inflammatory disorders has been documented. Epigenetic and endoplasmic reticulum stress are also observed in diabetic nephropathy. Targeting inflammation pathway and endoplasmic reticulum stress in podocytes may offer potential therapies to prevent the progression of diabetic nephropathy.
FRONTIERS IN IMMUNOLOGY
(2022)
Article
Pharmacology & Pharmacy
Qianqian Yang, Wenjia Xie, Xiao Wang, Jing Luo, Yang Zhou, Hongdi Cao, Qi Sun, Lei Jiang, Junwei Yang
Summary: The study discovered that early treatment with SS31 can protect podocytes and alleviate the development of DKD by inhibiting OMA1-mediated hydrolysis of OPA1.
FRONTIERS IN PHARMACOLOGY
(2022)
Review
Pharmacology & Pharmacy
Erina Sugita, Kaori Hayashi, Akihito Hishikawa, Hiroshi Itoh
Summary: Epigenetic alterations in podocytes are associated with chronic kidney disease, including diabetic nephropathy. Detection of these changes may serve as a promising strategy for estimating kidney damage and prognosis. Targeting epigenetic podocyte changes and associated DNA damage could be a novel therapeutic approach for preventing progression to end-stage renal disease in diabetic nephropathy patients.
FRONTIERS IN PHARMACOLOGY
(2021)
Article
Physiology
Yingying Zhang, Chengxian Xu, Qing Ye, Lingxiao Tong, Hong Jiang, Xiujuan Zhu, Limin Huang, Weiqiang Lin, Haidong Fu, Jingjing Wang, Pontus B. Persson, En Yin Lai, Jianhua Mao
Summary: The study demonstrated that in diabetic nephropathy, BASP1 activates the p53 pathway through co-repression with WT1, leading to podocyte apoptosis.
Article
Pharmacology & Pharmacy
Yiqi Liu, Yuan Li, Liu Xu, Jiasen Shi, Xiujuan Yu, Xue Wang, Xizhi Li, Hong Jiang, Tingting Yang, Xiaoxing Yin, Lei Du, Qian Lu
Summary: This study confirmed the anti-apoptotic effect of quercetin on podocyte apoptosis and demonstrated that it attenuated apoptosis by inhibiting the EGFR signaling pathway. These findings provide a novel approach to further investigate the mechanism of quercetin in the treatment of diabetic nephropathy.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Shuo Wang, Yakun Yang, Xingyu He, Lin Yang, Jianrong Wang, Shunjie Xia, Dan Liu, Shuxia Liu, Li Yang, Wei Liu, Huijun Duan
Summary: This study demonstrated that in diabetic conditions, the overactivity of Cdk5 leads to podocyte injury and mitochondrial dysfunction, whereas inhibition of Cdk5 can attenuate these injuries and dysfunctions by modulating Sirt1 phosphorylation. This suggests that Cdk5 may be a potential therapeutic target for the treatment of DN.
ANTIOXIDANTS & REDOX SIGNALING
(2021)