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Cadmium exposure induces renal fibrosis by inhibiting hsa_circ_0075684/miR-363-3p/KLF4 signaling pathway
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  • Published: 13 February 2026

Cadmium exposure induces renal fibrosis by inhibiting hsa_circ_0075684/miR-363-3p/KLF4 signaling pathway

  • Jiazhen Zhou1 na1,
  • Yiqi Huang2 na1,
  • Guoliang Li1,
  • Zhiqiang Zhao1,
  • Yaotang Deng1,
  • Siming Xian1,
  • Yue Hu1,
  • Mushi Yi1 &
  • …
  • Lili Liu  ORCID: orcid.org/0000-0001-7733-76541 

Scientific Reports , Article number:  (2026) Cite this article

We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Subjects

  • Biomarkers
  • Mechanisms of disease

Abstract

To date, no effective chelation therapy exists to remove cadmium (Cd) from the kidneys, a condition that increases the risk of cadmium-induced chronic kidney disease among humans. consequently, it is vital to prevent kidney damage due to cadmium exposure. However, it has been challenging to identify an early diagnostic marker of cadmium-induced kidney damage through mechanism studies. Interestingly, our previous study revealed that the expression of the microRNA miR-363-3p was upregulated in workers who had been diagnosed with chronic occupational cadmium toxicity. Thus, we aimed to investigate the role of miR-363-3p and its potential signaling pathway in cadmium-induced kidney damage. In this study, we identified a novel signaling pathway, hsa_circ_0075684/miR-363-3p/Krüppel-Like Factor 4 (KLF4), through a comprehensive bioinformatics analysis involving six databases. Next, we validated the role of the hsa_circ_0075684/miR-363-3p/KLF4 pathway in human renal tubular epithelial cell line (HK-2) treated with 0, 5, 10 and 15 µM cadmium chloride (CdCl2). Reverse transcription quantitative PCR (RT-qPCR) and western blot analyses showed that cadmium exposure induced renal fibrosis by regulating the expression of classic renal fibrosis biomarkers, including Fibronectin (Fn), E-cadherin (E-cad) and α-smooth muscle actin (α-SMA) through hsa_circ_0075684/miR-363-3p/KLF4 pathway inhibition. In a mice subchronic model (treated with 0, 5, 10 and 20 mg/kg CdCl2), Masson’s staining revealed obvious renal fibrosis in mice treated with 5, 10 and 20 mg/kg CdCl2 compared to the control group. The altered expression of hsa_circ_0075684/miR-363-3p/KLF4 pathway components and classic renal fibrosis biomarkers in model mice exposed to cadmium was consistent with that observed in HK-2 cells. In summary, we first report hsa_circ_0075684/miR-363-3p/KLF4 axis in cadmium nephrotoxicity, positioning it as a potential early diagnostic marker for cadmium-induced renal fibrosis.

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Data availability

All data used and/or analysed during the current study available from the corresponding author on reasonable request. E-mail: lli257@163.com.

Abbreviations

Cd:

Cadmium

CdCl2:

Cadmium chloride

RT-qPCR:

Reverse transcription quantitative PCR

Fn:

Fibronectin

E-cad:

E-cadherin

α-SMA:

α-Smooth muscle actin

CKD:

Chronic kidney disease

PI3K:

Phosphoinositide 3-kinase

CTD:

Comparative toxicogenomics database

GTEx:

Genotype-tissue expression

circRNA:

Circular RNA

MYLIP:

Myosin regulatory light chain interacting protein

GO:

Gene Ontology

KEGG:

Kyoto encyclopedia of genes and genomes

KLF4:

Krüppel-like factor 4

ANP32E:

Acidic nuclear phosphoprotein 32 family member E

COL1A2:

Collagen type I alpha 2 chain

ITGA5:

Integrin subunit alpha 5

UTRs:

Untranslated regions

WT:

Wilde type

MUT:

Mutant

TPM:

Transcripts per million

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Acknowledgements

HK-2 cells (human proximal tubule epithelial cell) were donated by Professor Wang Qing (School of Public Health, Sun Yat-sen University, China).Professional English language editing support was provided by AsiaEdit (asiaedit.com).

Funding

This research was supported by the National Natural Science Foundation of China (No. 81972990), Key Scientific Research Project Fund of GDHOD (Z2022-13 and Z2023-07), the Guangdong Provincial Natural Science Foundation (2024A1515012530 and 2024A1515013198), The "Guangdong Special Support Program" for Outstanding Young Talents (0820250239).

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  1. Jiazhen Zhou and Yiqi Huang contributed equally to this work.

Authors and Affiliations

  1. Department of Toxicology, Guangdong Province Hospital for Occupational Disease Prevention and·Treatment, Guangzhou, 510300, China

    Jiazhen Zhou, Guoliang Li, Zhiqiang Zhao, Yaotang Deng, Siming Xian, Yue Hu, Mushi Yi & Lili Liu

  2. Guang Zhou Haizhu Maternity and Child Health Hospital, Guang Zhou, 510240, China

    Yiqi Huang

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Contributions

YiQi Huang: Writing – original draft, Visualisation, Methodology, Investigation, Formal analysis. Jiazhen Zhou: Writing – review & editing, Project administration, Methodology, Investigation, Formal analysis, Conceptualisation. Lili Liu: Supervision, Funding acquisition, Conceptualisation. Guoliang Li, Zhiqiang Zhao and Yaotang Deng: Writing – review & editing, Investigation. Siming Xian, Yue Hu and Mushi Yi: Writing – review & editing, Investigation, Conceptualisation.

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Correspondence to Lili Liu.

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Zhou, J., Huang, Y., Li, G. et al. Cadmium exposure induces renal fibrosis by inhibiting hsa_circ_0075684/miR-363-3p/KLF4 signaling pathway. Sci Rep (2026). https://doi.org/10.1038/s41598-026-39715-w

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  • Received: 28 May 2025

  • Accepted: 06 February 2026

  • Published: 13 February 2026

  • DOI: https://doi.org/10.1038/s41598-026-39715-w

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Keywords

  • hsa_circ_0075684/miR-363-3p/KLF4
  • Cadmium
  • Renal fibrosis
  • Circular RNA
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