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JAK/STAT 通路在纤维化疾病中的作用：分子和细胞机制。

The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms.

机构信息

Department of Pulmonary and Critical Care Medicine, West China Hospital, Sichuan University, Chengdu 610041, China.

Laboratory of Pulmonary Immunology and Inflammation, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu 610041, China.

出版信息

Biomolecules. 2023 Jan 6;13(1):119. doi: 10.3390/biom13010119.

DOI:10.3390/biom13010119
PMID:36671504
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9855819/
Abstract

There are four members of the JAK family and seven of the STAT family in mammals. The JAK/STAT molecular pathway could be activated by broad hormones, cytokines, growth factors, and more. The JAK/STAT signaling pathway extensively mediates various biological processes such as cell proliferation, differentiation, migration, apoptosis, and immune regulation. JAK/STAT activation is closely related to growth and development, homeostasis, various solid tumors, inflammatory illness, and autoimmune diseases. Recently, with the deepening understanding of the JAK/STAT pathway, the relationship between JAK/STAT and the pathophysiology of fibrotic diseases was noticed, including the liver, renal, heart, bone marrow, and lung. JAK inhibitor has been approved for myelofibrosis, and subsequently, JAK/STAT may serve as a promising target for fibrosis in other organs. Therefore, this article reviews the roles and mechanisms of the JAK/STAT signaling pathway in fibrotic diseases.

摘要

哺乳动物中有四个 JAK 家族成员和七个 STAT 家族成员。JAK/STAT 分子途径可被广泛的激素、细胞因子、生长因子等激活。JAK/STAT 信号通路广泛介导多种生物学过程，如细胞增殖、分化、迁移、凋亡和免疫调节。JAK/STAT 的激活与生长发育、内稳态、各种实体瘤、炎症性疾病和自身免疫性疾病密切相关。最近，随着对 JAK/STAT 通路的深入了解，人们注意到 JAK/STAT 与纤维化疾病的病理生理学之间存在关联，包括肝脏、肾脏、心脏、骨髓和肺部。JAK 抑制剂已被批准用于骨髓纤维化，随后，JAK/STAT 可能成为其他器官纤维化的有希望的靶点。因此，本文综述了 JAK/STAT 信号通路在纤维化疾病中的作用和机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5d/9855819/e470600a4032/biomolecules-13-00119-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5d/9855819/b4a1413aa940/biomolecules-13-00119-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5d/9855819/475ba409c1e7/biomolecules-13-00119-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5d/9855819/ac207541d3ca/biomolecules-13-00119-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5d/9855819/e470600a4032/biomolecules-13-00119-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5d/9855819/b4a1413aa940/biomolecules-13-00119-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5d/9855819/475ba409c1e7/biomolecules-13-00119-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5d/9855819/ac207541d3ca/biomolecules-13-00119-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5d/9855819/e470600a4032/biomolecules-13-00119-g004.jpg

相似文献

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The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms.

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[6]
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本文引用的文献

[1]
Noncanonical JAK1/STAT3 interactions with TGF-β modulate myofibroblast transdifferentiation and fibrosis.

Am J Physiol Lung Cell Mol Physiol. 2022-12-1

[2]
The JAK/STAT pathway is activated in systemic sclerosis and is effectively targeted by tofacitinib.

J Scleroderma Relat Disord. 2020-2

[3]
The JAK/STAT signaling pathway: from bench to clinic.

Signal Transduct Target Ther. 2021-11-26

[4]
Necroptosis contributes to chronic inflammation and fibrosis in aging liver.

Aging Cell. 2021-12

[5]
The rationale for targeting the JAK/STAT pathway in scleroderma-associated interstitial lung disease.

Immunotherapy. 2021-2

[6]
Fibrosis: from mechanisms to medicines.

Nature. 2020-11

[7]
Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 to Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution.

Pharmacol Rev. 2020-4

[8]
STAT Signaling in Glioma Cells.

Adv Exp Med Biol. 2020

[9]
Synthesis and biological activity of thieno[3,2-d]pyrimidines as potent JAK3 inhibitors for the treatment of idiopathic pulmonary fibrosis.

Bioorg Med Chem. 2020-1-15

[10]
Retraction Note: Interactions between Th1 cells and Tregs affect regulation of hepatic fibrosis in biliary atresia through the IFN-γ/STAT1 pathway.

Cell Death Differ. 2020-7

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