ZLN005 Alleviates In Vivo and In Vitro Renal Fibrosis via PGC-1 alpha-Mediated Mitochondrial Homeostasis
文献类型：期刊论文
| 作者 | Zhu, Pengfei1,3,4; Ma, Haijian1; Cui, Shichao1; Zhou, Xiqiao4; Xu, Weilong4; Yu, Jiangyi3,4; Li, Jingya1,2
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| 刊名 | PHARMACEUTICALS
 |
| 出版日期 | 2022-04-01 |
| 卷号 | 15期号:4页码:14 |
| 关键词 | ZLN005 PGC-1 alpha mitochondrial homeostasis UUO |
| DOI | 10.3390/ph15040434 |
| 通讯作者 | Yu, Jiangyi(yujiangyi2007@163.com) ; Li, Jingya(jyli@simm.ac.cn) |
| 英文摘要 | Currently, chronic kidney disease (CKD) is one of the most common diseases; it is also a serious threat to human health due to its high mortality, and its treatment is still a major clinical challenge. Mitochondrial dyshomeostasis plays an important role in the development of CKD. ZLN005 is a novel peroxisome-proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1 alpha) activator from our laboratory. To explore whether ZLN005 can protect against CKD in vivo and in vitro, a unilateral ureteral obstruction (UUO) model and TGF-beta 1-treated renal tubular epithelial cells (TECs), respectively, were used in this study. We found that ZLN005-administrated UUO mice showed less kidney damages than control mice, as indicated by the reduced expression of fibrotic biomarkers in the kidney of UUO mice. ZLN005 treatment also alleviated the TGF-beta 1-induced fibrotic phenotype and lipid accumulation in TECs. Our study demonstrated ZLN005 treatment improved mitochondrial homeostasis at least partially via the activation of PGC-1 alpha, thus maintaining mitochondria function and energy homeostasis. In summary, ZLN005 treatment ameliorates UUO-induced renal fibrosis, providing conceptional support for mitochondria-targeting therapies for chronic kidney disease. |
| WOS关键词 | ACTIVATED RECEPTOR-ALPHA ; FATTY-ACID OXIDATION ; ACUTE KIDNEY INJURY ; BETA-OXIDATION ; DYSFUNCTION ; MICE ; PROGRESSION ; MECHANISMS ; EXPRESSION ; PROTECTION |
| 资助项目 | National Program on Key Research Project[2016YFC1305505] ; Shanghai Commission of Science and Technology[21S11907600] ; Shanghai Commission of Science and Technology[19431908100] |
| WOS研究方向 | Pharmacology & Pharmacy |
| 语种 | 英语 |
| 出版者 | MDPI |
| WOS记录号 | WOS:000785477000001 |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/299785]  |
| 专题 | 新药研究国家重点实验室 |
| 通讯作者 | Yu, Jiangyi; Li, Jingya |
| 作者单位 | 1.Chinese Acad Sci, Natl Ctr Drug Screening, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 201203, Peoples R China 2.Univ Chinese Acad Sci, Sch Pharmaceut Sci & Technol, Hangzhou Inst Adv Study, Hangzhou 310000, Peoples R China 3.Nanjing Univ Chinese Med, First Clin Med Sch, Nanjing 210000, Peoples R China 4.Nanjing Univ Chinese Med, Jiangsu Prov Hosp Chinese Med, Dept Endocrinol, Affiliated Hosp, Nanjing 210000, Peoples R China |
| 推荐引用方式 GB/T 7714 | Zhu, Pengfei,Ma, Haijian,Cui, Shichao,et al. ZLN005 Alleviates In Vivo and In Vitro Renal Fibrosis via PGC-1 alpha-Mediated Mitochondrial Homeostasis[J]. PHARMACEUTICALS,2022,15(4):14. |
| APA | Zhu, Pengfei.,Ma, Haijian.,Cui, Shichao.,Zhou, Xiqiao.,Xu, Weilong.,...&Li, Jingya.(2022).ZLN005 Alleviates In Vivo and In Vitro Renal Fibrosis via PGC-1 alpha-Mediated Mitochondrial Homeostasis.PHARMACEUTICALS,15(4),14. |
| MLA | Zhu, Pengfei,et al."ZLN005 Alleviates In Vivo and In Vitro Renal Fibrosis via PGC-1 alpha-Mediated Mitochondrial Homeostasis".PHARMACEUTICALS 15.4(2022):14. |
入库方式： OAI收割
来源：上海药物研究所
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