1,115
Views
11
CrossRef citations to date
0
Altmetric
Research Paper

Jixuepaidu Tang-1 inhibits epithelial-mesenchymal transition and alleviates renal damage in DN mice through suppressing long non-coding RNA LOC498759

, , , , &
Pages 3125-3136 | Received 14 Jun 2019, Accepted 23 Aug 2019, Published online: 29 Sep 2019

References

  • Ling L, Tan Z, Zhang C, et al. Long noncoding RNA ENSRNOG00000037522 is involved in the podocyte epithelial‑mesenchymal transition in diabetic rats. Int J Mol Med. 2018;41:2704–2714.
  • Dai H, Liu Q, Liu B. Research progress on mechanism of podocyte depletion in diabetic nephropathy. J Diabetes Res. 2017;2017:2615286.
  • Loeffler I, Wolf G. Epithelial-to-mesenchymal transition in diabetic nephropathy: fact or fiction? Cells. 2015;4:631–652.
  • Yamaguchi Y, Iwano M, Suzuki D, et al. Epithelial-mesenchymal transition as a potential explanation for podocyte depletion in diabetic nephropathy. Am J Kidney Dis. 2009;54:653–664.
  • Wang X, Xu Y, Zhu YC, et al. LncRNA NEAT1 promotes extracellular matrix accumulation and epithelial-to-mesenchymal transition by targeting miR-27b-3p and ZEB1 in diabetic nephropathy. J Cell Physiol. 2019;234:12926–12933.
  • Gao J, Wang W, Wang F, et al. LncRNA-NR_033515 promotes proliferation, fibrogenesis and epithelial-to-mesenchymal transition by targeting miR-743b-5p in diabetic nephropathy. Biomed Pharmacothe. 2018;106:543–552.
  • Chen YN, Wu CG, Shi BM, et al. The protective effect of asiatic acid on podocytes in the kidney of diabetic rats. Am J Transl Res. 2018;10:3733–3741.
  • Alqahtani A, Hamid K, Kam A, et al. The pentacyclic triterpenoids in herbal medicines and their pharmacological activities in diabetes and diabetic complications. Curr Med Chem. 2013;20:908–931.
  • Liao H, Hu L, Cheng X, et al. Are the therapeutic effects of huangqi (Astragalus membranaceus) on diabetic nephropathy correlated with its regulation of macrophage iNOS activity? J Immunol Res. 2017;2017:3780572.
  • Kim J, Moon E, Kwon S. Effect of Astragalus membranaceus extract on diabetic nephropathy. Endocrinol Diabetes Metab Case Rep. 2014;2014:140063.
  • Wang Z, Sun WS, Liu JT. Impacts of asiaticoside on cytoskeleton and p38 pathway in podocytes (in Chinese). World J Integr Tradit West Med. 2015;10:1456–1459.
  • Ramesh BN, Girish TK, Raghavendra RH, et al. Comparative study on anti-oxidant and anti-inflammatory activities of Caesalpinia crista and Centella asiatica leaf extracts. J Pharm Bioallied Sci. 2014;6:86–91.
  • Zhai R, Jian G, Chen T, et al. Astragalus membranaceus and Panax notoginseng, the novel renoprotective compound, synergistically protect against podocyte injury in streptozotocin-induced diabetic rats. J Diabetes Res. 2019;2019:1602892.
  • Hu CM, Li JS, Cheah KP, et al. Effect of Sanguis draconis (a dragon’s blood resin) on streptozotocin- and cytokine-induced beta-cell damage, in vitro and in vivo. Diabetes Res Clin Pract. 2011;94:417–425.
  • Li Y, Ren D, Xu G. Long noncoding RNA MALAT1 mediates high glucose-induced glomerular endothelial cell injury by epigenetically inhibiting klotho via methyltransferase G9a. IUBMB Life. 2019;71:873–881.
  • Shen H, Ming Y, Xu C, et al. Deregulation of long noncoding RNA (TUG1) contributes to excessive podocytes apoptosis by activating endoplasmic reticulum stress in the development of diabetic nephropathy. J Cell Physiol. 2019;234:15123–15133.
  • Lu H, Chen B, Hong W, et al. Transforming growth factor-beta1 stimulates hedgehog signaling to promote epithelial-mesenchymal transition after kidney injury. Febs J. 2016;283:3771–3790.
  • Lu X, Li M, Zhou L, et al. Urinary serum- and glucocorticoid-inducible kinase SGK1 reflects renal injury in patients with immunoglobulin A nephropathy. Nephrology (Carlton, Vic). 2014;19:307–317.
  • Liu W, Wang X, Wang Y, et al. SGK1 inhibition-induced autophagy impairs prostate cancer metastasis by reversing EMT. J Exp Clin Cancer Res. 2018;37:73.
  • Hills CE, Squires PE. TGF-beta1-induced epithelial-to-mesenchymal transition and therapeutic intervention in diabetic nephropathy. Am J Nephrol. 2010;31:68–74.
  • Sun Z, Ma Y, Chen F, et al. miR-133b and miR-199b knockdown attenuate TGF-beta1-induced epithelial to mesenchymal transition and renal fibrosis by targeting SIRT1 in diabetic nephropathy. Eur J Pharmacol. 2018;837:96–104.
  • Feng Y, Wang Q, Wang Y, et al. SGK1-mediated fibronectin formation in diabetic nephropathy. Cell Physiol Biochem. 2005;16:237–244.
  • Cheng J, Truong LD, Wu X, et al. Serum- and glucocorticoid-regulated kinase 1 is upregulated following unilateral ureteral obstruction causing epithelial-mesenchymal transition. Kidney Int. 2010;78:668–678.
  • Zhao Y, Yin Z, Li H, et al. MiR-30c protects diabetic nephropathy by suppressing epithelial-to-mesenchymal transition in db/db mice. Aging Cell. 2017;16:387–400.
  • Yue Y, Meng K, Pu Y, et al. Transforming growth factor beta (TGF-beta) mediates cardiac fibrosis and induces diabetic cardiomyopathy. Diabetes Res Clin Pract. 2017;133:124–130.
  • Loeffler I. MKP2 suppresses TGF-beta1-induced epithelial-to-mesenchymal transition through JNK inhibition. Clin Sci. 2019;133:545–550.
  • Kim J-H, Ham S, Lee Y, et al. TTC3 contributes to TGF-β(1)-induced epithelial-mesenchymal transition and myofibroblast differentiation, potentially through SMURF2 ubiquitylation and degradation. Cell Death Dis. 2019;10:92.
  • Lu Q, Wang WW, Zhang MZ, et al. ROS induces epithelial-mesenchymal transition via the TGF-beta1/PI3K/Akt/mTOR pathway in diabetic nephropathy. Exp Ther Med. 2019;17:835–846.
  • Lang F, Bohmer C, Palmada M, et al. (Patho)physiological significance of the serum- and glucocorticoid-inducible kinase isoforms. Physiol Rev. 2006;86:1151–1178.
  • Steinberger M, Foller M, Vogelgesang S, et al. Lack of the serum- and glucocorticoid-inducible kinase SGK1 improves muscle force characteristics and attenuates fibrosis in dystrophic mdx mouse muscle. Pflugers Arch. 2015;467:1965–1974.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.