HO-1:纤维化的新目标。

IF 4.5 2区 生物学 Q2 CELL BIOLOGY
Chenxi Lu, Yuan Liu, Feifei Ren, Haoran Zhang, Yafang Hou, Hong Zhang, Zhiyong Chen, Xia Du
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引用次数: 0

摘要

纤维化是一种对组织损伤的异常修复反应,涉及细胞外基质合成和降解之间平衡的破坏,导致细胞外基质在正常组织内过度积累,最终导致器官功能障碍。纤维化表现为几乎所有慢性疾病的晚期阶段,死亡率很高,对人类健康构成重大威胁。血红素加氧酶-1(HEME oxygenase-1,HO-1)是一种内源性保护剂,通过其抗氧化、抗炎和抗细胞凋亡的特性减轻组织损伤。大量研究证实,HO-1 具有作为抗纤维化治疗靶点的潜力。本综述深入探讨了 HO-1 的结构和功能属性以及上下游途径。此外,还阐明了 HO-1 在纤维化相关细胞中的调控网络和机制。此外,还探讨了 HO-1 在各种纤维化相关疾病中的作用。总之,这些全面的信息为未来的研究奠定了基础,并增强了HO-1作为纤维化治疗靶点的可行性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
HO-1: An emerging target in fibrosis.

Fibrosis, an aberrant reparative response to tissue injury, involves a disruption in the equilibrium between the synthesis and degradation of the extracellular matrix, leading to its excessive accumulation within normal tissues, and culminating in organ dysfunction. Manifesting in the terminal stages of nearly all chronic ailments, fibrosis carries a high mortality rate and poses a significant threat to human health. Heme oxygenase-1 (HO-1) emerges as an endogenous protective agent, mitigating tissue damage through its antioxidant, anti-inflammatory, and antiapoptotic properties. Numerous studies have corroborated HO-1's potential as a therapeutic target in anti-fibrosis treatment. This review delves into the structural and functional attributes, and the upstream and downstream pathways of HO-1. Additionally, the regulatory networks and mechanisms of HO-1 in cells associated with fibrosis are elucidated. The role of HO-1 in various fibrosis-related diseases is also explored. Collectively, this comprehensive information serves as a foundation for future research and augments the viability of HO-1 as a therapeutic target for fibrosis.

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来源期刊
CiteScore
14.70
自引率
0.00%
发文量
256
审稿时长
1 months
期刊介绍: The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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