Department of Nephrology, The First Hospital of Jilin University, 1 Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, People's Republic of China.
Physical Examination Center, The First Hospital of Jilin University, 1 Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, People's Republic of China.
Int Urol Nephrol. 2022 Aug;54(8):1881-1889. doi: 10.1007/s11255-022-03118-3. Epub 2022 Jan 20.
Renal fibrosis (RF) is the main pathological feature of chronic kidney disease (CKD). The main focus of research on treatment for CKD is to develop strategies that delay or prevent RF from progressing to end-stage renal disease (ESRD). Inflammation and oxidative stress occur during all stages of CKD. The magnesium cation (Mg) can reduce inflammation and oxidative stress, regulate apoptosis, and improve RF, and magnesium-based therapies are promising new treatments that can prevent RF. We reviewed the current evidence on the effects of magnesium in RF and examined the possible mechanism of magnesium in delaying RF.
We searched PubMed, Web of Science, and EMBASE for articles on magnesium and fibrosis, with a focus on magnesium and RF.
Inflammation, oxidative stress, and apoptosis are related to the occurrence of CKD. Previous research showed that Mg inhibits the differentiation of inflammatory cells, down-regulates the production of inflammatory cytokines, reduces inflammation, and reduces the production of reactive oxygen species (ROS) and oxidative stress. In addition, Mg also regulates apoptosis and protects renal tubular function. Magnesium may also regulate TRPM6/7, promote the secretion of klotho protein and improve renal fibrosis. Therefore, Mg can protect the kidney from damage and slow down the progression of RF through many molecular and cellular effects. Some of the anti-fibrotic effects of Mg may be related to its antagonism of intracellular Ca.
Magnesium may prevent the progression of renal fibrosis and delay CKD by reducing renal inflammation and oxidative stress, and by regulating fibrosis-related signaling pathways and cytokines.
肾纤维化（RF）是慢性肾脏病（CKD）的主要病理特征。CKD 治疗研究的主要重点是开发延迟或阻止 RF 进展为终末期肾病（ESRD）的策略。在 CKD 的所有阶段都会发生炎症和氧化应激。镁阳离子（Mg）可以减轻炎症和氧化应激，调节细胞凋亡，并改善 RF，基于镁的治疗方法是有前途的新治疗方法，可以预防 RF。我们回顾了镁在 RF 中的作用的现有证据，并研究了镁在延迟 RF 中的可能机制。
我们在 PubMed、Web of Science 和 EMBASE 上搜索了关于镁和纤维化的文章，重点是镁和 RF。
炎症、氧化应激和细胞凋亡与 CKD 的发生有关。先前的研究表明，Mg 抑制炎症细胞的分化，下调炎症细胞因子的产生，减轻炎症，减少活性氧（ROS）的产生和氧化应激。此外，Mg 还调节细胞凋亡并保护肾小管功能。镁还可能调节 TRPM6/7，促进 klotho 蛋白的分泌并改善肾纤维化。因此，Mg 通过多种分子和细胞作用可以保护肾脏免受损伤并减缓 RF 的进展。Mg 的一些抗纤维化作用可能与其对细胞内 Ca 的拮抗作用有关。
镁可能通过减轻肾脏炎症和氧化应激，调节纤维化相关信号通路和细胞因子，来预防肾纤维化的进展并延缓 CKD。
