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  4. Vol 4, Issue 1, 2023

TGF- β Study on the Role of Iron Death Signal Transduction in Diabetes Nephropathy

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DOI: 10.23977/medsc.2023.040112 | Downloads: 31 | Views: 344

Author(s)

Hua Xiao 1, Hongbao Liu 2

Affiliation(s)

1 Shaanxi University of Chinese Medicine, Xianyang, 712046, China
2 Department of Nephrology, Tangdu Hospital, Air Force Military Medical University (Fourth Military Medical University), Xi'an, 710038, China

Corresponding Author

Hongbao Liu

ABSTRACT

DN (Diabetes Nephropathy) is the result of multiple factors, and its pathogenesis is complex. Extensive evidence has proven TGF- β. It plays an important role in the pathogenesis of DN, but the specific way of action is still unclear. TGF- β after binding and activating its receptor, its signal transmission needs to be carried out by a series of post receptor signal molecules TGF- β. It is the last and common important mediator of kidney damage caused by changes in biochemical factors and cytokines, such as blood glucose rise in diabetes. It can directly lead to DN characteristic pathological changes such as renal cell hypertrophy, excessive accumulation of extracellular matrix, glomerulosclerosis, renal interstitial fibrosis, etc. In DN, TGF- β the characteristic function of the β - lactamase is to stimulate the matrix deposition in the mesangial region. Through TGF- β. Further study on the role of DN iron death signal transduction in diabetes islets β the research on the mechanism of cell injury is reviewed. At the same time, it can not only increase the synthesis of extracellular matrix, but also inhibit the degradation of extracellular matrix components.

KEYWORDS

TGF-β, Diabetic nephropathy, Iron death, Signal conduction

CITE THIS PAPER

Hua Xiao, Hongbao Liu, TGF- β Study on the Role of Iron Death Signal Transduction in Diabetes Nephropathy. MEDS Clinical Medicine (2023) Vol. 4: 72-77. DOI: http://dx.doi.org/10.23977/medsc.2023.040112.

REFERENCES

[1] Hu Y, Liu S, Liu W, et al. Bioinformatics analysis of genes related to iron death in diabetic nephropathy through network and pathway levels based approaches [J]. PLoS ONE, 2021, 16(11): e0259436-e0259468.
[2] Rafiee Z, Orazizadeh M, Nejad Dehbashi F, et al. Mesenchymal stem cells derived from the kidney can ameliorate diabetic nephropathy through the TGF-β/Smad signaling pathway [J]. Environmental Science and Pollution Research, 2022, 29(35): 53212-53224.
[3] Zheng W, Qian C, Xu F, et al. Fuxin Granules ameliorate diabetic nephropathy in db/db mice through TGF-β1/Smad and VEGF/VEGFR2 signaling pathways [J]. Biomedicine & Pharmacotherapy, 2021, 141(3): 111806-111848.
[4] Pang R, Gu D. Triptolide Improves Renal Injury in Diabetic Nephropathy Rats through TGF-β1/Smads Signal Pathway [J]. Endocrine, metabolic & immune disorders drug targets, 2021, 38(10): 21-58.
[5] Chen X, Sun L, Li D, et al. Green tea peptides ameliorate diabetic nephropathy by inhibiting the TGF-β/Smad signaling pathway in mice [J]. Food & Function, 2022, 13(15): 14-36.
[6] Wang X B, Zhu H, Song W, et al. Gremlin Regulates Podocyte Apoptosis via Transforming Growth Factor-β (TGF-β) Pathway in Diabetic Nephropathy [J]. Med Sci Monit, 2018, 24(11): 183-189.
[7] Wang L, Wang Z, Yang Z, et al. Study of the Active Components and Molecular Mechanism of Tripterygium wilfordii in the Treatment of Diabetic Nephropathy [J]. Frontiers in Molecular Biosciences, 2021, 8.
[8] Mohammed M E, Abbas A M, Badi R M, et al. Effect of Acacia senegal on TGF-β1 and vascular mediators in a rat model of diabetic nephropathy [J]. Archives of Physiology and Biochemistry, 2020, 28(2): 1-11.
[9] Ma Y, Shi J, Wang F, et al. MiR‐130b increases fibrosis of HMC cells by regulating the TGF‐β1 pathway in diabetic nephropathy [J]. Journal of Cellular Biochemistry, 2018, 120(26): 33-48.
[10] Jin D, Jia M, Xie Y, et al. Impact of klotho on the expression of SRGAP2a in podocytes in diabetic nephropathy [J]. BMC Nephrology, 2022, 23(26): 11-23.

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