Evidence map›Paper›PMID 42325768›Full record

ArticleAmerican journal of translational research2026

Single-nucleus transcriptomics identifies SPON1 as a candidate mediator of the anti-fibrotic effect of

Chaoyu Zhu, Zhen Zhu, Renjie Wang, Yuanyuan Xiao, Qianqian Wang, Xinyi Wang, Jun Yin, Li Wei

Abstract read
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Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Chaoyu ZhuDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Clinical Center for Diabetes, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus Shanghai 200233, China.
Zhen ZhuDepartment of Respiratory Medicine, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai 200233, China.
Renjie WangSchool of Basic Medicine, Chongqing Medical University Chongqing 400016, China.
Yuanyuan XiaoDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Clinical Center for Diabetes, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus Shanghai 200233, China.
Qianqian WangDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Clinical Center for Diabetes, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus Shanghai 200233, China.
Xinyi WangDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Clinical Center for Diabetes, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus Shanghai 200233, China.
Jun YinDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Clinical Center for Diabetes, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus Shanghai 200233, China.
Li WeiDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Clinical Center for Diabetes, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus Shanghai 200233, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThis study elucidated the cell-type-specific mechanisms and molecular targets underlying the anti-fibrotic effects of

methodsDKD was induced in C57BL/6J mice by a high-fat diet and streptozotocin. Mice received oral AM extract (2.0 g/kg/day) for 14 weeks. We performed snRNA-seq on control, DKD, and AM-treated kidneys, utilizing computational tools to infer intercellular communication. Validation was conducted using quantitative real-time polymerase chain reaction (qRT-PCR), immunohistochemistry, western blotting, and confocal microscopy.

resultsAM significantly reduced the urinary albumin-to-creatinine ratio and ameliorated glomerular and interstitial fibrosis in DKD mice. snRNA-seq identified proximal tubular segment 1 and interstitial cell clusters as the primary responders to AM. The extract suppressed transforming growth factor-beta TGF-β/Smad-related profibrotic signaling and remodeled epithelial-stromal intercellular communication by downregulating C-X-C motif chemokine ligand (CXCL) and colony-stimulating factor (CSF) pathways. Notably, spondin 1 (SPON1), an extracellular matrix-associated matricellular protein, was among the most significantly downregulated genes. Consistent with these findings, SPON1 expression was markedly reduced in both DKD kidneys and HG-injured HK-2 cells following AM administration.

conclusionsAM attenuates diabetic renal fibrosis by reducing SPON1 expression, suppressing profibrotic signaling, and remodeling epithelial-stromal crosstalk. These findings provide cell-type-resolved insights into AM's renoprotective mechanisms and highlight SPON1 as a candidate molecular target in DKD.

Indexed as

Abelmoschus manihot (L.)diabetic kidney diseaseepithelial-stromal interactionrenal fibrosissingle-nucleus RNA sequencingSPON1

Identifiers

PMID42325768
PMCPMC13275808

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