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HIPK2作为纤维化的新型调节因子。

HIPK2 as a Novel Regulator of Fibrosis.

作者信息

Garufi Alessia, Pistritto Giuseppa, D'Orazi Gabriella

机构信息

Unit of Cellular Networks, Department of Research and Advanced Technologies, IRCCS Regina Elena National Cancer Institute, 00144 Rome, Italy.

Centralized Procedures Office, Italian Medicines Agency (AIFA), 00187 Rome, Italy.

出版信息

Cancers (Basel). 2023 Feb 7;15(4):1059. doi: 10.3390/cancers15041059.

DOI:10.3390/cancers15041059
PMID:36831402
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9954661/
Abstract

Fibrosis is an unmet medical problem due to a lack of evident biomarkers to help develop efficient targeted therapies. Fibrosis can affect almost every organ and eventually induce organ failure. Homeodomain-interacting protein kinase 2 (HIPK2) is a protein kinase that controls several molecular pathways involved in cell death and development and it has been extensively studied, mainly in the cancer biology field. Recently, a role for HIPK2 has been highlighted in tissue fibrosis. Thus, HIPK2 regulates several pro-fibrotic pathways such as Wnt/β-catenin, TGF-β and Notch involved in renal, pulmonary, liver and cardiac fibrosis. These findings suggest a wider role for HIPK2 in tissue physiopathology and highlight HIPK2 as a promising target for therapeutic purposes in fibrosis. Here, we will summarize the recent studies showing the involvement of HIPK2 as a novel regulator of fibrosis.

摘要

由于缺乏明显的生物标志物来帮助开发有效的靶向治疗方法,纤维化是一个尚未解决的医学问题。纤维化几乎可以影响每个器官,并最终导致器官衰竭。同源结构域相互作用蛋白激酶2(HIPK2)是一种蛋白激酶,它控制着涉及细胞死亡和发育的多种分子途径,并且已经得到了广泛研究,主要是在癌症生物学领域。最近,HIPK2在组织纤维化中的作用受到了关注。因此,HIPK2调节多种促纤维化途径,如参与肾、肺、肝和心脏纤维化的Wnt/β-连环蛋白、TGF-β和Notch途径。这些发现表明HIPK2在组织生理病理学中具有更广泛的作用,并突出了HIPK2作为纤维化治疗靶点的潜力。在此,我们将总结最近的研究,这些研究表明HIPK2作为纤维化的新型调节因子发挥了作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/91ffbff15544/cancers-15-01059-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/c346dde94a7b/cancers-15-01059-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/41f726899cde/cancers-15-01059-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/cfb2b6cba0ae/cancers-15-01059-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/e45d3f30ba15/cancers-15-01059-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/1623404feeb7/cancers-15-01059-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/8ed45d36c8cb/cancers-15-01059-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/91ffbff15544/cancers-15-01059-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/c346dde94a7b/cancers-15-01059-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/41f726899cde/cancers-15-01059-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/cfb2b6cba0ae/cancers-15-01059-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/e45d3f30ba15/cancers-15-01059-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/1623404feeb7/cancers-15-01059-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/8ed45d36c8cb/cancers-15-01059-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1df/9954661/91ffbff15544/cancers-15-01059-g007.jpg

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