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Cullin-associated and neddylation-dissociated protein 1 (CAND1) promotes cardiomyocyte proliferation and heart regeneration by enhancing the ubiquitinated degradation of Mps one binder kinase activator 1b (Mob1b)

Cell Death & Differentiation volume 32, pages 2384–2398 (2025)Cite this article

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Abstract

Activation of the intrinsic regenerative potential of adult mammalian hearts by promoting cardiomyocyte proliferation holds great potential in heart repair. CAND1 (Cullin-associated and neddylation-dissociated protein 1) functions as a critical regulator of cellular protein homeostasis by fine-tuning the ubiquitinated degradation of specific abnormally expressed protein substrates. Here, we identified that cardiac-specific transgenic overexpression of CAND1 reduced the infarct size, restored cardiac function, and promoted cardiomyocyte proliferation after myocardial infarction in juvenile (7-day-old) and adult (8-week-old) mice. Conversely, CAND1 deficiency blunted the regenerative capacity of neonatal hearts after apex resection. MS and functional verification demonstrated that CAND1 enhanced the assembly of Cullin1, FBXW11(F-box/WD repeat-containing protein 11), and Mob1b (Mps one binder kinase activator 1b) complexes, and thus promotes the degradation of Mob1b. The ubiquitination of Mob1b occurred at K108 and was linked by K48 of ubiquitin. Mob1b deletion partially rescued the loss of regenerative capacity in neonatal hearts induced by CAND1 deficiency and improved cardiac function in adult mice post-MI. Moreover, CAND1 promoted the proliferation of human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). Our data demonstrate that CAND1 promotes cardiomyocyte proliferation via FBXW11-mediated K48-linked ubiquitination degradation of Mob1b, and improves heart regeneration after cardiac injury. The findings provide a novel strategy to promote cardiac regeneration and repair.

Schematic diagram of the role of CAND1 in regulating ubiquitination and degradation of Mob1b and cardiomyocyte proliferation and heart regeneration. Under CAND1-High condition, CAND1 promotes the incorporation of Cullin1, FBXW11, and Mob1b complexes, and accelerates SCFFBXW11-mediated K48-linked ubiquitination of Mob1b at the K108 site, which leads to the degradation of Mob1b and thus suppresses the Hippo signaling pathway and facilitates cardiomyocyte proliferation and heart regeneration post-MI.

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Fig. 1: CAND1 was upregulated during neonatal heart regeneration and promoted cardiomyocyte proliferation.
Fig. 2: CAND1 overexpression improved functional recovery, repairment, and cardiomyocyte proliferation of the MI heart at the adult stage (8-week-old) of mice.
Fig. 3: CAND1 depletion impaired cardiac regeneration in neonatal mice.
Fig. 4: CAND1 regulates the ubiquitination and degradation of Mob1b.
Fig. 5: CAND1 promotes the formation of Cullin1, FBXW11, and Mob1b complexes.
Fig. 6: K108 is important for K48-linked ubiquitination of FBXW11 mediated by Mob1b.
Fig. 7: CAND1 regulates cardiomyocyte proliferation via Mob1b.
Fig. 8: CAND1 increases the proliferation of human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs).

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Data availability

All data generated or analyzed during this study are included in this published article and its Supplementary Information files. Additional supporting data are available from the corresponding authors upon reasonable request.

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Funding

This work was supported by the Ministry of Science and Technology of China (YFA1800902 to ZP), National Natural Science Foundation of China (82430017, 82270245 to ZP, 82170393, 82470308 to YZ, 82070283 to YL, and 82330011, U21A20339 to BFY), Natural Science Foundation of Heilongjiang (LH2023H047 to XDL), and China Postdoctoral Science Foundation (2023MD744212 to XDL), Spring Goose Support Program: Young Talents Project funding of Heilongjiang Province (CYQN24041 to YZ).

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Author notes

  1. These authors contributed equally: Xingda Li, Lingmin Zhang, Tao Tian.

Authors and Affiliations

  1. National Key Laboratory of Frigid Zone Cardiovascular Diseases, Department of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education. International Cooperation Base for Major Cardiovascular Diseases in Cold Regions, China), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, PR China

    Xingda Li, Lingmin Zhang, Tao Tian, Yao Pei, Kaile Wang, Shuang Wang, Xuan Ning, Pinhan Zhao, Yueying Qu, Haiyu Gao, Chenhong Li, Xuening Liu, Jiming Yang, Yingzi Zhang, Hongbin Gao, Lina Xuan, Yang Zhang, Yanjie Lu, Benzhi Cai, Baofeng Yang & Zhenwei Pan

  2. Department of Pharmacy at the Second Affiliated Hospital, and Department of Pharmacology at College of Pharmacy (The Key Laboratory of Cardiovascular Research, Ministry of Education), Harbin Medical University, Harbin, China

    Xingda Li

  3. Research Unit of Noninfectious Chronic Diseases in Frigid Zone, Chinese Academy of Medical Sciences, 2019 Research Unit 070, Harbin, Heilongjiang, PR China

    Zhenwei Pan

  4. Key Laboratory of Cell Transplantation, The First Affiliated Hospital, Harbin Medical University, Harbin, China

    Zhenwei Pan

  5. School of Basic Medical Sciences, Harbin Medical University, Harbin, China

    Zhenwei Pan

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  1. Xingda Li
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Contributions

WP, BY, BC, and YL conceived the study concept. XL, LZ, and TT performed the animal experiments, conducted Western blot and qPCR analysis. YP, KW, and SW performed the histological examination of mice heart samples. XN, PZ, YQ, and HG performed cell culture. CL, XL, JY, and YZ helped culture hiPSCs-derived cardiomyocytes. HG, LX, and YZ performed IF staining. XL, LZ, and TT carried out the data analysis. WP and XL wrote the manuscript. WP and BY provided the funding. All authors reviewed the manuscript.

Corresponding authors

Correspondence to Yanjie Lu, Benzhi Cai, Baofeng Yang or Zhenwei Pan.

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The authors declare no competing interests.

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Throughout the study, all experiments involving animals were approved by the Ethics Committees of Harbin Medical University and conformed to the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH Publication No. 85–23, revised 1996). Mice in the experiment were randomly assigned to experimental groups using computer-generated randomization. All experiments were permitted by the Animal Care and Use Committee of Harbin Medical University.

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Li, X., Zhang, L., Tian, T. et al. Cullin-associated and neddylation-dissociated protein 1 (CAND1) promotes cardiomyocyte proliferation and heart regeneration by enhancing the ubiquitinated degradation of Mps one binder kinase activator 1b (Mob1b). Cell Death Differ 32, 2384–2398 (2025). https://doi.org/10.1038/s41418-025-01540-5

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