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International Journal of Molecular Medicine
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Print ISSN: 1107-3756 Online ISSN: 1791-244X
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September-2026 Volume 58 Issue 3

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Article Open Access

circCACNA1D drives pulmonary fibrosis by regulating pyruvate kinase M2 dimer‑tetramer switching

  • Authors:
    • Yujie Wang
    • Xiaoting Li
    • Meirong Wang
    • Nailiang Zhai
    • Mengqi Jiang
    • Bo Liu
    • Changjun Lv
    • Songzi Zhang
    • Xiaodong Song
    • Jinjin Zhang

  • View Affiliations / Copyright

    Affiliations: Department of Cellular and Genetic Medicine, Shandong Key Laboratory of Complex Medical Intelligence and Aging, Shandong Medical and Pharmaceutical University, Yantai, Shandong 264003, P.R. China, Department of Medical Laboratory, Yantai Affiliated Hospital of Shandong Medical and Pharmaceutical University, Yantai, Shandong 264000, P.R. China, Department of Respiratory and Critical Care Medicine, Shandong Medical and Pharmaceutical University Hospital, Shandong Medical and Pharmaceutical University, Binzhou, Shandong 256603, P.R. China
    Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 260
    |
    Published online on: July 15, 2026
       https://doi.org/10.3892/ijmm.2026.5931
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Abstract

Pulmonary fibrosis is a progressive and fatal interstitial lung disease characterized by aberrant fibroblast activation and excessive extracellular matrix deposition. Circular RNAs (circRNAs) have emerged as critical regulators of fibrotic pathogenesis. However, their mechanistic roles remain incompletely defined. In the present study, circCACNA1D was identified as a novel driver of pulmonary fibrosis progression through direct interaction with pyruvate kinase M2 (PKM2). Specifically, circCACNA1D binds PKM2 and promotes its nuclear translocation and dimerization. This process is facilitated by desuccinylation at conserved lysine residues (K135, K166 and K270). The conformational shift from the tetrameric to the dimeric state reprograms cellular metabolism toward aerobic glycolysis and activates a pro‑fibrotic transcriptional program, including direct upregulation of KIF4A. In addition, the pharmacological stabilization of PKM2 tetramers with TEPP‑46 attenuated fibrotic phenotypes in vitro and alleviated bleomycin‑induced pulmonary fibrosis in mice. These findings define a previously unrecognized circRNA‑driven axis that coordinates PKM2 conformational switching, metabolic reprogramming and transcriptional activation, and suggest a potential therapeutic strategy for pulmonary fibrosis.

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Copy and paste a formatted citation
Spandidos Publications style
Wang Y, Li X, Wang M, Zhai N, Jiang M, Liu B, Lv C, Zhang S, Song X, Zhang J, Zhang J, et al: circCACNA1D drives pulmonary fibrosis by regulating pyruvate kinase M2 dimer‑tetramer switching. Int J Mol Med 58: 260, 2026.
APA
Wang, Y., Li, X., Wang, M., Zhai, N., Jiang, M., Liu, B. ... Zhang, J. (2026). circCACNA1D drives pulmonary fibrosis by regulating pyruvate kinase M2 dimer‑tetramer switching. International Journal of Molecular Medicine, 58, 260. https://doi.org/10.3892/ijmm.2026.5931
MLA
Wang, Y., Li, X., Wang, M., Zhai, N., Jiang, M., Liu, B., Lv, C., Zhang, S., Song, X., Zhang, J."circCACNA1D drives pulmonary fibrosis by regulating pyruvate kinase M2 dimer‑tetramer switching". International Journal of Molecular Medicine 58.3 (2026): 260.
Chicago
Wang, Y., Li, X., Wang, M., Zhai, N., Jiang, M., Liu, B., Lv, C., Zhang, S., Song, X., Zhang, J."circCACNA1D drives pulmonary fibrosis by regulating pyruvate kinase M2 dimer‑tetramer switching". International Journal of Molecular Medicine 58, no. 3 (2026): 260. https://doi.org/10.3892/ijmm.2026.5931
Copy and paste a formatted citation
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Spandidos Publications style
Wang Y, Li X, Wang M, Zhai N, Jiang M, Liu B, Lv C, Zhang S, Song X, Zhang J, Zhang J, et al: circCACNA1D drives pulmonary fibrosis by regulating pyruvate kinase M2 dimer‑tetramer switching. Int J Mol Med 58: 260, 2026.
APA
Wang, Y., Li, X., Wang, M., Zhai, N., Jiang, M., Liu, B. ... Zhang, J. (2026). circCACNA1D drives pulmonary fibrosis by regulating pyruvate kinase M2 dimer‑tetramer switching. International Journal of Molecular Medicine, 58, 260. https://doi.org/10.3892/ijmm.2026.5931
MLA
Wang, Y., Li, X., Wang, M., Zhai, N., Jiang, M., Liu, B., Lv, C., Zhang, S., Song, X., Zhang, J."circCACNA1D drives pulmonary fibrosis by regulating pyruvate kinase M2 dimer‑tetramer switching". International Journal of Molecular Medicine 58.3 (2026): 260.
Chicago
Wang, Y., Li, X., Wang, M., Zhai, N., Jiang, M., Liu, B., Lv, C., Zhang, S., Song, X., Zhang, J."circCACNA1D drives pulmonary fibrosis by regulating pyruvate kinase M2 dimer‑tetramer switching". International Journal of Molecular Medicine 58, no. 3 (2026): 260. https://doi.org/10.3892/ijmm.2026.5931
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