Evidence map›Paper›PMID 41663594›Full record

ArticleFunctional & integrative genomics2026

Honokiol attenuates renal fibrosis via SIRT3-Mediated regulation of Wnt/β-Catenin signaling.

Zihao Guo, Jing Wang, Xing Li, Xiang Ren, Yisheng Yin, Yiqun Tian, Zhenliang Qin, Kun Yuan, Xiaoyong Zeng

Abstract read
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In one paragraph

Article in Functional & integrative genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Zihao Guo *Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1095 Jiefang Avenue, Wuhan, 430030, China.
Jing Wang *Institute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Key Laboratory of Organ Transplantation, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Huazhong University of Science and Technology, Ministry of Education, Chinese Academy of Medical Sciences, Wuhan, China.
Xing LiDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1095 Jiefang Avenue, Wuhan, 430030, China.
Xiang RenDepartment of Urology, Xijing Hospital, Air Force Medical University, Xi'an, China.
Yisheng YinDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1095 Jiefang Avenue, Wuhan, 430030, China.
Yiqun TianDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1095 Jiefang Avenue, Wuhan, 430030, China.
Zhenliang QinDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1095 Jiefang Avenue, Wuhan, 430030, China.
Kun YuanDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1095 Jiefang Avenue, Wuhan, 430030, China.
Xiaoyong ZengDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1095 Jiefang Avenue, Wuhan, 430030, China. xiaoyong3zeng@outlook.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal fibrosis, a mutual pathological manifestation of chronic kidney disease (CKD), currently has limited therapeutic options. Honokiol (HKL), a polyphenolic compound isolated from Magnolia officinalis, has demonstrated anti-fibrotic effects; however, its molecular mechanisms remain incompletely characterized. The anti-fibrotic effect of HKL was investigated using the unilateral ureteral obstruction (UUO) mouse framework in vivo and transforming growth factor-β1 (TGF-β1)-stimulated HK2 cells in vitro, followed by HKL treatment and assessed by fibrosis markers and signalling axis. Conditional Sirtuin 3 (SIRT3) knockout (cKO) mice and SIRT3 siRNA-transfected HK2 cells were utilised to investigate the function of SIRT3 in mediating HKL’s anti-fibrotic impacts. HKL significantly attenuated renal fibrosis, reducing the deposition of extracellular matrix (ECM) and reversing epithelial-mesenchymal transition. Mechanistically, HKL-activated SIRT3 downregulated Wnt/β-catenin signaling axis, evidenced by decreased nuclear β-catenin accumulation and a subsequent reduction in transcriptional activity, which refers to the activation of fibrosis-related genetic factors like Collagen I, Fibronectin, and α-SMA upon β-catenin binding to TCF/LEF transcription factors. SIRT3 deficiency restored Wnt/β-catenin signaling axis activation and eliminated anti-fibrotic impacts of HKL. HKL mitigates renal fibrosis via SIRT3-mediated suppression of Wnt/β-catenin signaling, proposing a novel targeted therapeutic strategy for CKD-associated fibrosis.

Indexed as

Biphenyl CompoundsKidney DiseasesLignansSirtuin 3Wnt Signaling PathwayAllyl CompoundsAnimalsbeta CateninCell LineEpithelial-Mesenchymal TransitionFibrosisHumansKidneyMaleMiceMice, KnockoutAllyl Compoundsbeta CateninBiphenyl CompoundshonokiolLignansPhenolsSirt3 protein, mouseSirtuin 3Chronic kidney diseaseHonokiolRenal fibrosisSirtuin 3The wnt/β-catenin signaling axis

Identifiers

PMID41663594

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.