家畜子宫内膜纤维化的细胞分子机制研究进展

doi:10.11843/j.issn.0366-6964.2024.06.006

Abstract

Abstract:

Endometrial fibrosis is caused by persistent damage stimulation of the endometrium leading to its impaired repair, characterized by excessive deposition of extracellular matrix, which may lead to endometrial structural damage and dysfunction or even failure of the endometrium, affecting the fertility and reproductive quality of domestic animals. Therefore, analyzing the formation mechanism of endometrial fibrosis is of significance for improving the fertility of domestic animals. This article elaborates on the trigger factors of endometrial fibrosis, the relationship between the cellular and molecular mechanisms of fibrosis formation, cellular metabolic regulation and extracellular matrix, further discusses the therapeutic strategies for fibrosis and future research directions aiming to provide a reference for the study of endometrial fibrosis in domestic animals.

Key words: endometrial fibrosis, extracellular matrix, myofibroblast, epithelial mesenchymal transition, stress, cellular metabolism

CLC Number:

S814

Tingting CHU, Xiaoyu ZHANG, Lei SUN, Jiashun TONG, Lei ZHANG, Yuxuan SONG. Advances in Cellular and Molecular Mechanisms of Endometrial Fibrosis in Domestic Animals[J]. Acta Veterinaria et Zootechnica Sinica, 2024, 55(6): 2334-2344.

Figures/Tables 3

References 88

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信号通路 Signaling pathway	靶向细胞 Targeted cells	调控因子 Regulators	参与纤维化的调控作用 Involved in the regulation of fibrosis	参考文献 Reference
TGF-β	上皮细胞、成纤维细胞	IL-17A、SMAD、RhoA、Ras、TAK1、P13K、mTOR	促进EMT，促进胶原蛋白和纤连蛋白的合成，促进谷氨酰胺分解	[51-53]
Hippo	成纤维细胞、肌成纤维细胞、	TAZ、YAP、Wnt、Smad	促进α-SMA和CTGF表达，调节干细胞的生长和分化，诱导COL1A1上调，调控成纤维细胞分化和ECM合成	[54, 60]
Hedgehog	基质细胞	CTGF、Gli1、Ptch1	促进肌成纤维细胞活化，诱导COL1A1、α-SMA表达	[54, 61]
PI3K/AKT	基质细胞	mTOR	促进基质细胞增殖分化、促进胶原沉积	[59, 62]
Wnt/β-Catenin	基质细胞	mTOR	促进αSMA、Col-I、FN和CTGF表达	[57-58]

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Advances in Cellular and Molecular Mechanisms of Endometrial Fibrosis in Domestic Animals

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