缺氧促进肾小管上皮细胞表达 ADAM9，从而增强 TGF-β1 的活化并促进狼疮性肾炎的组织纤维化

IF 11.4 1区医学 Q1 RHEUMATOLOGY

Arthritis & Rheumatology Pub Date : 2024-09-15 DOI:10.1002/art.42987

Masataka Umeda, Kohei Karino, Abhigyan Satyam, Nobuya Yoshida, Ryo Hisada, Rhea Bhargava, Theodoros Vichos, Ana Laura Kunzler, Takashi Igawa, Kunihiro Ichinose, Kenta Torigoe, Tomoya Nishino, Takahiro Maeda, Caroline A. Owen, Reza Abdi, Atsushi Kawakami, George C. Tsokos

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引用次数: 0

摘要

狼疮性肾炎（LN）患者肾脏中转化生长因子-β（TGF-β）的表达增强会导致肾脏进行性纤维化，造成终末器官损伤。分解蛋白和金属蛋白酶 9（ADAM9）通过裂解潜伏相关肽（LAP）来激活 TGF-β1。我们推测，肾脏中的 ADAM9 可通过激活 TGF-β1 加速纤维化。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Hypoxia Promotes the Expression of ADAM9 by Tubular Epithelial Cells which Enhances TGF-β1 Activation and Promotes Tissue Fibrosis in Lupus Nephritis

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Hypoxia Promotes the Expression of ADAM9 by Tubular Epithelial Cells which Enhances TGF-β1 Activation and Promotes Tissue Fibrosis in Lupus Nephritis

Enhanced expression of transforming growth factor-beta (TGF-β) in the kidneys of patients with lupus nephritis (LN) can lead to progressive fibrosis, resulting in end-organ damage. Disintegrin and metalloproteinases 9 (ADAM9) activate TGF-β1 by cleaving the latency-associated peptide (LAP). We hypothesized that ADAM9 in the kidney may accelerate fibrogenesis by activating TGF-β1.

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来源期刊

Arthritis & Rheumatology RHEUMATOLOGY-

CiteScore

20.90

自引率

3.00%

发文量

371

期刊介绍： Arthritis & Rheumatology is the official journal of the American College of Rheumatology and focuses on the natural history, pathophysiology, treatment, and outcome of rheumatic diseases. It is a peer-reviewed publication that aims to provide the highest quality basic and clinical research in this field. The journal covers a wide range of investigative areas and also includes review articles, editorials, and educational material for researchers and clinicians. Being recognized as a leading research journal in rheumatology, Arthritis & Rheumatology serves the global community of rheumatology investigators and clinicians.