The Research Progress of TGF-β in Obstructive Renal Water
DOI:
https://doi.org/10.54097/49rg4j69Keywords:
TGF-β1, Obstructive Kidney Accumulation, Kidney FibrosisAbstract
Transformation and growth factor β (TGF-β) is a newly discovered TGF-β super family that regulates cell growth and differentiation. Obstructive renal hydrophilic water causes the kidney unit to be damaged, and the renal function will also decrease. In the end, the kidneys are in a non-functional state, causing many harms to the physical and mental health of patients. Finders that can promote cell fibrosis, and play a key role in the pathological development of chronic kidney disease. TGF-β1 participates in various processes, including promoting multi-energy stem cells into fibroblasts, stimulating kidney capillaries endothelial cells, polygonal shapes, polygonal shapes Cells and mesenchymal cells are converted into fibroblasts. Through the research on the TGF-β structure, type, synthesis, signal transition, and its relationship with renal fibrosis, it helps to reveal its role in renal fibrosis. This article will review the latest research progress of the pathogenesis of TGF-β in the pathogenesis of obstructive renal water hydrosis and treatment, in order to propose the latest research conclusions of obstructive kidney accumulation diagnosis and treatment, which provides theoretical guidance for the treatment of obstructive renal water.
Downloads
References
[1] Chen Jie. The analysis of the influencing factors of the recovery of the recovery of the renal function after the destruction of the severe renal water obstruction [D]. Zunyi Medical University, 2022.
[2] Bo S, Sedaghat F, Pavuluri K, et al. Dynamic Contrast Enhanced-MR CEST Urography: An Emerging Tool in the Diagnosis and Management of Upper Urinary Tract Obstruction[J]. Tomography, 2021,7(1):80-94.
[3] Zhu Li, Ding Longhui, Shi Weifeng. GFR combined with serum CYS C, β_2-Mg to varying degrees of diagnostic value for patients with water accumulation [J]. Molecular diagnosis and treatment magazine, 2023,15 (01): 157-160.
[4] Hu Jian, Peng Qiang. Poor pelvic formation under the laparoscopic pelvic pelvis on severe congenital renal water surgical indicators, pain scores and prognosis [J]. PLA pharmaceutical magazine, 2021, 33 (03): 87 -90.
[5] Jin B, Zhu J, Zhou Y, et al. Loss of MEN1 leads to renal fibrosis and decreases HGF-Adamts5 pathway activity via an epigenetic mechanism[J]. Clin Transl Med, 2022,12(8): e982.
[6] Ten D P, Arthur H M. Extracellular control of TGFbeta signalling in vascular development and disease[J]. Nat Rev Mol Cell Biol, 2007,8(11):857-869.
[7] Robertson I B, Rifkin D B. Regulation of the Bioavailability of TGF-β and TGF-β-Related Proteins[J]. Cold Spring Harb Perspect Biol, 2016,8(6).
[8] Miyazono K, Heldin C H. Role for carbohydrate structures in TGF-beta 1 latency[J]. Nature, 1989,338(6211):158-160.
[9] Jung Y S, Kim Y H, Radhakrishnan K, et al. Orphan nuclear receptor ERRγ regulates hepatic TGF-β2 expression and fibrogenic response in CCl(4)-induced acute liver injury[J]. Arch Toxicol, 2021,95(9):3071-3084.
[10] Yuan Q, Tang B, Zhang C. Signaling pathways of chronic kidney diseases, implications for therapeutics[J]. Signal Transduct Target Ther, 2022,7(1):182.
[11] Groppe J, Hinck C S, Samavarchi-Tehrani P, et al. Cooperative assembly of TGF-beta superfamily signaling complexes is mediated by two disparate mechanisms and distinct modes of receptor binding[J]. Mol Cell, 2008,29(2):157-168.
[12] Gipson G R, Goebel E J, Hart K N, et al. Structural perspective of BMP ligands and signaling[J]. Bone, 2020,140:115549.
[13] Huse M, Muir T W, Xu L, et al. The TGF beta receptor activation process: an inhibitor- to substrate-binding switch [J]. Mol Cell, 2001,8(3):671-682.
[14] Ram C, Gairola S, Syed A M, et al. Biochanin A alleviates unilateral ureteral obstruction-induced renal interstitial fibrosis and inflammation by inhibiting the TGF-β1/Smad2/3 and NF-kB/NLRP3 signaling axis in mice[J]. Life Sci, 2022,298: 120 527.
[15] Jiang M, Bai M, Xu S, et al. Blocking AURKA with MK-5108 attenuates renal fibrosis in chronic kidney disease[J]. Biochim Biophys Acta Mol Basis Dis, 2021,1867(11):166227.
[16] Ai K, Li X, Zhang P, et al. Genetic or siRNA inhibition of MBD2 attenuates the UUO- and I/R-induced renal fibrosis via downregulation of EGR1[J]. Mol Ther Nucleic Acids, 2022, 28:77-86.
[17] Kuppe C, Ibrahim M M, Kranz J, et al. Decoding myofibroblast origins in human kidney fibrosis[J]. Nature, 2021,589 (7841): 281-286.
[18] Yu X Y, Sun Q, Zhang Y M, et al. TGF-β/Smad Signaling Pathway in Tubulointerstitial Fibrosis[J]. Front Pharmacol, 2022,13:860588.
[19] Liu L, Zhang P, Bai M, et al. p53 upregulated by HIF-1α promotes hypoxia-induced G2/M arrest and renal fibrosis in vitro and in vivo[J]. J Mol Cell Biol, 2019,11(5):371-382.
[20] Chen X, Yu C, Hou X, et al. Histone deacetylase 6 inhibition mitigates renal fibrosis by suppressing TGF-β and EGFR signaling pathways in obstructive nephropathy[J]. Am J Physiol Renal Physiol, 2020,319(6): F1003-F1014.
[21] Kim I Y, Lee M Y, Park M W, et al. Deletion of Akt1 Promotes Kidney Fibrosis in a Murine Model of Unilateral Ureteral Obstruction[J]. Biomed Res Int, 2020,2020:6143542.
[22] Yang Y, Feng X, Liu X, et al. Fate alteration of bone marrow-derived macrophages ameliorates kidney fibrosis in murine model of unilateral ureteral obstruction[J]. Nephrol Dial Transplant, 2019,34(10):1657-1668.
[23] Zhang X, Li L X, Yu C, et al. Targeting lysine-specific demethylase 1A inhibits renal epithelial-mesenchymal transition and attenuates renal fibrosis[J]. FASEB J, 2022,36 (1):e22122.
[24] Gwon M G, An H J, Gu H, et al. Apamin inhibits renal fibrosis via suppressing TGF-β1 and STAT3 signaling in vivo and in vitro[J]. J Mol Med (Berl), 2021,99(9):1265-1277.
Downloads
Published
Issue
Section
License
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
How to Cite
