WNT5A通过FOXP1促进缺血再灌注损伤诱导的急性肾损伤向慢性肾脏病转化的机制研究

doi:10.3969/j.issn.1674-8115.2026.07.006

上海交通大学学报（医学版） ›› 2026, Vol. 46 ›› Issue (7): 875-885.doi: 10.3969/j.issn.1674-8115.2026.07.006

• 论著 · 基础研究 • 上一篇

WNT5A通过FOXP1促进缺血再灌注损伤诱导的急性肾损伤向慢性肾脏病转化的机制研究

俸浩然, 刘君君, 王恺纯, 汪年松, 顾思捷(), 范瑛()

上海交通大学医学院附属第六人民医院肾内科，上海 200233

收稿日期:2026-03-31 接受日期:2026-05-08 出版日期:2026-07-28 发布日期:2026-07-28
通讯作者: 范　瑛，主任医师，博士；电子信箱：fanyingsh@126.com。
顾思捷，博士；电子信箱：illusion1997@qq.com。
基金资助:
国家自然科学基金(82570825);国家自然科学基金(82270761);上海交通大学“交大之星”医工交叉重点项目(YG2023ZD21);上海交通大学医学院“双百人”项目(20192833);国家科技重大专项(2024ZD0523400);国家科技重大专项(2024ZD0523404)

Mechanism of WNT5A in aggravating the ischemia-reperfusion injury-induced acute kidney injury to chronic kidney disease transition by promoting FOXP1

Feng Haoran, Liu Junjun, Wang Kaichun, Wang Niansong, Gu Sijie(), Fan Ying()

Department of Nephrology, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200233, China

Received:2026-03-31 Accepted:2026-05-08 Online:2026-07-28 Published:2026-07-28
Contact: Fan Ying, E-mail: fanyingsh@126.com.
Gu Sijie, E-mail: illusion1997@qq.com. ^#Co-corresponding authors.
Supported by:
National Natural Science Foundation of China(82570825);Key Project of “SJTU Trans-med Awards Research” Medical-Engineering Integration Research Fund in Shanghai Jiao Tong University(YG2023ZD21);“Two-hundred Talents” Program of Shanghai Jiao Tong University School of Medicine(20192833);National Science and Technology Major Project of China(2024ZD0523400)

摘要/Abstract

摘要：

目的·研究无翅型MMTV整合位点家族成员5A（wingless-type MMTV integration site family member 5A，WNT5A）促进缺血再灌注损伤（ischemia-reperfusion injury，IRI）诱导的急性肾损伤（acute kidney injury，AKI）向慢性肾脏病（chronic kidney disease，CKD）转化的机制。方法·在野生型小鼠中构建IRI诱导的AKI向CKD转化模型，造模第3和第14日时，取肾脏组织行苏木精-伊红（H-E）染色观察组织病理损伤，Masson染色、免疫组织化学染色检测Ⅰ型胶原蛋白α1（collagen type Ⅰ α1 chain，COL1A1）以评估纤维化程度，同时通过转录组测序、实时荧光定量PCR（real-time quantitative PCR，qPCR）、Western blotting定量Wnt5a表达水平。构建Wnt5a杂合敲除（Wnt5a^+/- ）小鼠，建立IRI诱导的AKI向CKD转化模型，检测血清肌酐及血尿素氮水平以评估肾功能，肾脏损伤和纤维化程度评估方式同上。在转化生长因子-β（transforming growth factor-β，TGF-β）诱导的人肾皮质近端肾小管上皮细胞系HK-2中过表达WNT5A，转录组测序后对差异表达基因行基因本体（Gene Ontology，GO）的生物学过程富集分析，筛选关键靶基因，并通过qPCR和Western blotting验证WNT5A对叉头框蛋白P1（forkhead box protein P1，FOXP1）的调控作用。在HK-2细胞中过表达FOXP1，或在过表达WNT5A时沉默FOXP1，通过qPCR和Western blotting检测NOTCH2（notch receptor 2）通路相关分子NOTCH2、HEY1（hairy/enhancer-of-split related with YRPW motif 1）和HES1（hairy and enhancer of split 1），及纤维化标志物COL1A1和波形蛋白（vimentin，VIM）mRNA和蛋白的表达。结果·IRI术后第3日，小鼠肾组织Wnt5a表达显著升高，伴肾小管明显扩张及炎症细胞浸润；术后第14日，Wnt5a表达进一步升高，肾纤维化标志物COL1A1显著上调。Wnt5a^+/- 小鼠与野生型小鼠相比，IRI术后第14日血清肌酐及血尿素氮水平显著下降，肾功能明显改善；同时FOXP1表达下调，肾小管损伤及肾脏纤维化程度减轻。在TGF-β诱导的HK-2细胞中过表达WNT5A可明显上调转录因子FOXP1的表达；转录组测序及GO富集分析提示纤维化及NOTCH通路显著激活。过表达FOXP1可上调HK-2细胞中NOTCH2及其下游靶点HEY1和HES1的表达，COL1A1和VIM的mRNA和蛋白表达也显著增加；反之，在WNT5A过表达的细胞中沉默FOXP1可逆转NOTCH2通路分子及纤维化标志物的上调。结论·WNT5A可上调转录因子FOXP1表达，进而激活NOTCH2信号通路，从而推动IRI诱导的AKI向CKD的转化进程，促进肾纤维化进展。

关键词: 急性肾损伤, 慢性肾脏病, 肾脏纤维化, 无翅型MMTV整合位点家族成员5A, 叉头框蛋白P1, NOTCH2

Abstract:

Objective ·To investigate the mechanism by which wingless-type MMTV integration site family member 5A (WNT5A) promotes the transition from ischemia-reperfusion injury (IRI)-induced acute kidney injury (AKI) to chronic kidney disease (CKD). Methods ·An IRI-induced AKI-to-CKD transition model was established in wild-type (WT) mice. Renal histopathological injury was assessed by hematoxylin-eosin (H-E) staining on the 3rd and the 14th day after IRI. Fibrosis was evaluated by Masson staining and immunohistochemistry for collagen type Ⅰ α1 chain (COL1A1). Wnt5a expression was quantified by RNA sequencing (RNA-seq), real-time quantitative PCR (qPCR), and Western blotting. Wnt5a heterozygous knockout (Wnt5a^+/- ) mice were used to establish the IRI-induced AKI-to-CKD transition model. Renal function was evaluated by serum creatinine (Scr) and blood urea nitrogen (BUN), and renal injury and fibrosis were assessed as described above. In vitro, a transforming growth factor-β (TGF-β)-induced fibrotic model was established in HK-2 cells (a human renal cortex proximal tubular epithelial cell line) with WNT5A overexpression. Differentially expressed genes identified by RNA-seq were subjected to Gene Ontology (GO) biological process enrichment analysis to identify key targets. Regulation of forkhead box protein P1 (FOXP1) by WNT5A was validated by qPCR and Western blotting. FOXP1 was overexpressed, or silenced in the context of WNT5A overexpression in HK-2 cells. Expression levels of notch receptor 2 (NOTCH2) pathway components, including NOTCH2, hairy/enhancer-of-split related with YRPW motif 1(HEY1), and hairy and enhancer of split 1 (HES1), as well as fibrosis markers, including COL1A1 and vimentin (VIM), were analyzed by qPCR and Western blotting. Results ·Wnt5a expression was increased in the renal tissue on the 3rd day after IRI, accompanied by marked tubular dilation and inflammatory cell infiltration. On the 14th day, Wnt5a expression was further increased, along with significant upregulation of fibrotic markers. Compared with WT mice, Wnt5a^+/- mice exhibited reduced Scr and BUN levels on the 14th day after IRI, indicating improved renal function. FOXP1 expression was decreased, and tubular injury and renal fibrosis were attenuated in Wnt5a^+/- mice. Mechanistically, WNT5A overexpression markedly upregulated FOXP1 in TGF-β-treated HK-2 cells. RNA-seq and GO analysis indicated significant enrichment of fibrosis-related processes and activation of the NOTCH signaling pathway. FOXP1 overexpression increased the mRNA and protein levels of NOTCH2 and its downstream targets HEY1 and HES1, along with elevated COL1A1 and VIM expression. In contrast, silencing FOXP1 in WNT5A-overexpressing cells reversed the upregulation of NOTCH2 pathway components and fibrosis markers. Conclusion ·WNT5A upregulates the transcription factor FOXP1, which activates the NOTCH2 signaling pathway, thereby accelerating the IRI-induced AKI-to-CKD transition, and promoting renal fibrosis progression.

Key words: acute kidney injury (AKI), chronic kidney disease (CKD), renal fibrosis, wingless-type MMTV integration site family member 5A (WNT5A), forkhead box protein P1 (FOXP1), notch receptor 2 (NOTCH2)

中图分类号:

R692.5

俸浩然, 刘君君, 王恺纯, 汪年松, 顾思捷, 范瑛. WNT5A通过FOXP1促进缺血再灌注损伤诱导的急性肾损伤向慢性肾脏病转化的机制研究[J]. 上海交通大学学报（医学版）, 2026, 46(7): 875-885.

Feng Haoran, Liu Junjun, Wang Kaichun, Wang Niansong, Gu Sijie, Fan Ying. Mechanism of WNT5A in aggravating the ischemia-reperfusion injury-induced acute kidney injury to chronic kidney disease transition by promoting FOXP1[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2026, 46(7): 875-885.

图/表 6

表1 qPCR引物序列

Tab 1 Primer sequences for qPCR

Gene	Sequence (5′→3′)
FOXP1 (human)	F: GGGGCAGTATGGACAGTGGATGA R: TTGAGAGGTGTGCAGTAGGCGTG
NOTCH2 (human)	F: CCTTCCACTGTGAGTGTCTGA R: AGGTAGCATCATTCTGGCAGG
HEY1 (human)	F: TCTGCTAAGCTAGAAAAAGCCG R: GTGCGCGTCAAAGTAACCT
HES1 (human)	F: TCAACACGACACCGGATAAAC R: GCCGCGAGCTATCTTTCTTCA
COL1A1 (human)	F: GTGCGATGACGTGATCTGTGA R: CGGTGGTTTCTTGGTCGGT
VIM (human)	F: GACGCCATCAACACCGAGTT R: CTTTGTCGTTGGTTAGCTGGT
β-actin (human)	F: AGAGCTACGAGCTGCCTGAC R: AGCACTGTGTTGGCGTACAG
Wnt5a (mouse)	F: CAACTGGCAGGACTTTCTCAA R: CATCTCCGATGCCGGAACT
Foxp1 (mouse)	F: TCTCGTCCTCGGCACCTT R: GTCACAAACCGCCTCACA
β-actin (mouse)	F: AGAGGGAAATCGTGCGTGACA R: CACTGTGTTGGCATAGAGGTC

图1 Wnt5a 在IRI诱导的AKI小鼠模型中的表达情况Note： A. Renal histological changes in Sham group and IRI group (D3 and D14) mice evaluated by H-E staining; collagen fiber deposition assessed by Masson′s trichrome staining and immunohistochemical staining of COL1A1 (×400, scale bar=20 μm). B. Quantification of fibrotic area (percentage of total tissue area) based on Masson′s trichrome staining from three non-overlapping independent fields (n=5). C. The average integrated optical density (IOD) of COL1A1 immunohistochemical staining quantified from three non-overlapping independent fields (n=5). D. Temporal changes in Wnt5a gene expression at different time points after IRI in mice (n=5). E. qPCR analysis of Wnt5a expression in Sham group and IRI group (D3 and D14) (n=5). F. Western blotting analysis of WNT5A expression in Sham group and IRI group (D3 and D14). G. Quantification of Western blotting results (n=5). ①P<0.001, ④P=0.024, compared with the IRI-D3 group; ②P<0.001, ③P=0.009, compared with the Sham group.

Fig 1 Expression of Wnt5a in the IRI-induced AKI mouse model

图2 敲除 Wnt5a 显著抑制IRI诱导的AKI小鼠向肾纤维化进展Note： A. Immunohistochemical staining of WNT5A, renal histological changes evaluated by H-E staining, and collagen fiber deposition assessed by Masson′s trichrome staining (×400, scale bar=20 μm). B. The average IOD of WNT5A immunohistochemical staining quantified from three non-overlapping independent fields (n=5). C. Quantification of fibrotic area (percentage of total tissue area) based on Masson′s trichrome staining from three non-overlapping independent fields (n=5). D. Quantification of Scr levels in the three groups (n=5). E. Quantification of BUN levels in the three groups (n=5). F. Western blotting analysis of WNT5A, COL1A1, and VIM expression in the three groups. G. Quantification of the Western blotting results (n=5). ①P<0.001, compared with the WT Sham group; ②P<0.001, ③P=0.004, ④P=0.011, ⑤P=0.015, ⑥P=0.013, compared with the WT IRI-D14 group.

Fig 2 Wnt5a knockout markedly attenuates renal fibrosis progression in IRI-induced AKI mice

图3 FOXP1是WNT5A介导的肾纤维化下游的关键调控靶点Note： A. Volcano plot of differentially expressed genes between WNT5A-overexpressing (OE) and control HK-2 cells (both treated with TGF-β). B. GO enrichment analysis of differentially expressed genes in the two groups of HK-2 cells. C. qPCR analysis of FOXP1 expression in the two groups of HK-2 cells. D. Western blotting analysis of WNT5A and FOXP1 expression in the two groups of HK-2 cells. E. Quantification of the Western blotting results shown in Figure D. F. Immunohistochemical staining of FOXP1 in WT Sham, WT IRI, and Wnt5a+/- IRI mice (×400, scale bar=20 μm). G. The average IOD of FOXP1 immunohistochemical staining quantified from three non-overlapping independent fields (n=5). H. qPCR analysis of Foxp1 expression in the three groups of mice (n=5). I. Western blotting analysis of FOXP1 expression in the three groups of mice. J. Quantification of the Western blotting results shown in Figure I (n=5). ①P<0.001, compared with the control HK-2 cells; ②P<0.001, ④P=0.003, compared with the WT Sham group; ③P<0.001, ⑤P=0.002, compared with the WT IRI-D14 group.

Fig 3 FOXP1 serves as a key downstream effector of WNT5A-mediated renal fibrosis

图4 FOXP1 过表达在HK-2纤维化诱导模型中通过NOTCH2通路上调纤维化标志物表达Note： A. qPCR analysis of NOTCH2, HEY1, HES1, COL1A1, and VIM expression in FOXP1-OE and control HK-2 cells (both treated with TGF-β). B. Western blotting analysis of FOXP1, NOTCH2, HEY1, HES1, COL1A1, and VIM expression in the two groups of cells. C. Quantification of the Western blotting results. ①P<0.001, ②P=0.003, ③P=0.004, compared with the control HK-2 cells.

Fig 4 FOXP1 overexpression upregulates the expression of fibrosis markers through the NOTCH2 pathway in TGF-β-treated HK-2 cells

图5 在 WNT5A 过表达的HK-2纤维化诱导细胞模型中沉默 FOXP1 可抑制NOTCH2通路并下调纤维化标志物表达Note： A. Western blotting analysis of WNT5A, FOXP1, NOTCH2, HEY1, HES1, COL1A1, and VIM expression in control, WNT5A-OE, and WNT5A-OE with FOXP1 silencing HK-2 cells (all treated with TGF-β). B. Quantification of the Western blotting results. ①P<0.001, ④P=0.014, ⑥P=0.007, compared with the control HK-2 cells; ②P<0.001, ③P=0.002, ⑤P=0.013, ⑦P=0.005, ⑧P=0.008, compared with the WNT5A-OE HK-2 cells.

Fig 5 Silencing FOXP1 in WNT5A-overexpressing TGF-β-treated HK-2 cells inhibits the NOTCH2 pathway and downregulates the expression of fibrotic markers

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WNT5A通过FOXP1促进缺血再灌注损伤诱导的急性肾损伤向慢性肾脏病转化的机制研究

Mechanism of WNT5A in aggravating the ischemia-reperfusion injury-induced acute kidney injury to chronic kidney disease transition by promoting FOXP1

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