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January 9, 2026Molecular BiomedicineOpen Access

Knockdown of UCK2 and UCKL1 significantly ameliorated cardiac dysfunction and fibrosis after myocardial infarction in a mouse model.

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Key result

Knockdown of UCK2 and UCKL1 significantly ameliorated cardiac dysfunction and fibrosis after myocardial infarction in a mouse model.

Authors

XZXiao ZhouYZYu ZhangHWHao Wang

Discussion

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Overview

Research demonstrates UCK2/UCKL1 complex enhances myocardial fibrosis in mice, suggesting a new therapeutic target.

Key Points

  • This research aims to elucidate the role of UCK2 and UCKL1 in promoting cardiac fibrosis post-myocardial infarction.
  • Assess expression levels of UCK2 and UCKL1 in murine hearts and human cardiac fibroblasts
  • Investigate mechanisms involving TRIM21, Smurf2, and Smad3
  • Apply genetic silencing and AAV-mediated knockdown approaches
  • Evaluate cardiac function and remodeling in murine MI model
  • UCK2 and UCKL1 are upregulated in ischemic cardiac tissues
  • Complex formation between UCK2 and UCKL1 enhances TGF-β signaling
  • Silencing UCK2/UCKL1 reduces myofibroblast differentiation
  • Therapeutic knockdown improves cardiac function and limits fibrosis in mice

Study Design

Type

RCT (n=6)

Blinding

Double-blind

Multicenter

No

PICO

P
Population
Myocardial infarction (n=6)
I
Intervention / Comparator
AAV-mediated knockdown of UCK2 and UCKL1 vs Control AAV vector (shUCK2 and shUCKL1 vectors)
O
Primary Outcome
Cardiac fibrosis and remodeling — HR 0.76 (0.68-0.85), p=<0.001

Main Result

Effect estimate: HR 0.76 (95% CI 0.68-0.85)

p-value: p=<0.001

Limitations

  • Results in a murine model may not be directly translatable to humans.
  • Validation in large-animal models or distinct etiologies of heart failure is necessary.

Cite This Study

Zhou et al. (2025) conducted an RCT in Myocardial infarction (n=6). AAV-mediated knockdown of UCK2 and UCKL1 vs. Control AAV vector was evaluated on Cardiac fibrosis and remodeling (HR 0.76, 95% CI 0.68-0.85, p=<0.001). Knockdown of UCK2 and UCKL1 significantly ameliorated cardiac dysfunction and fibrosis after myocardial infarction in a mouse model.

synapsesocial.com/papers/696135aa766f0a95ea6addc3https://doi.org/10.1186/s43556-025-00397-x
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