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November 11, 2025Acta Biochimica et Biophysica Sinica2 citationsOpen Access

CDC5L facilitates cardiomyocyte proliferation and ameliorates myocardial ischemia-reperfusion injury via modulation of the FGF10-YAP axis

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Why the study?

Does CDC5L overexpression improve myocardial regeneration and reduce ischemia-reperfusion injury in mouse models?

Population

In vitro oxygen-glucose deprivation/reoxygenation model in neonatal mouse cardiomyocytes and in vivo…

Comparison

Modulation of CDC5L expression via adenoviral or… vs Control

Design

Preclinical

Key result

CDC5L overexpression attenuated cardiac ischemia-reperfusion injury by promoting cardiomyocyte proliferation and inhibiting apoptosis through the FGF10-YAP pathway.

Authors

TWTianwen WeiYSYuxiao SunYLYucheng Liang

Discussion

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Member takes

Overview

Hypothesis-generating for CDC5L as a myocardial regeneration target; leaves open translation to human ischemia-reperfusion injury.

Structured PICO

Does CDC5L overexpression improve myocardial regeneration and reduce ischemia-reperfusion injury in mouse models?

P
Population
Neonatal mouse cardiomyocytes and adult mice subjected to in vitro oxygen-glucose deprivation/reoxygenation and in vivo ischemia-reperfusion injury.
I
Intervention
Modulation of CDC5L expression via adenoviral or AAV9-mediated overexpression or knockdown
C
Comparator
Control (implied, not explicitly detailed in abstract)
O
Outcome
Cardiomyocyte proliferation (EdU+, Ki67+, pH3+), apoptosis (TUNEL staining, Bax/Bcl-2 ratio), cardiac function (echocardiography), and infarct sizesurrogate

CDC5L attenuates cardiac ischemia-reperfusion injury by promoting cardiomyocyte proliferation and inhibiting apoptosis through the FGF10-YAP pathway, representing a potential therapeutic target for myocardial regeneration.

Cite This Study

Wei et al. (2025) studied Myocardial ischemia-reperfusion injury. CDC5L overexpression or knockdown was evaluated on Cardiomyocyte proliferation, apoptosis, and cardiac function. CDC5L overexpression attenuated cardiac ischemia-reperfusion injury by promoting cardiomyocyte proliferation and inhibiting apoptosis through the FGF10-YAP pathway.

synapsesocial.com/papers/6aa2632a259d37a6a5e56579https://doi.org/10.3724/abbs.2025213
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Also Consider

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  1. 1LMCD1 aggravates cardiac fibrosis after myocardial infarction via activating STAT5A.2026
  2. 2Abstract Thu007: C5ORF51/RIMOC1 is Required for Adult Cardiomyocyte Maturation and Quiescence2025
  3. 3Abstract Wed004: Growth Differentiation Factor 11 Regulates Cardiomyocyte Cycling After Myocardial Infarction2025
  4. 4FGF10 promotes regional foetal cardiomyocyte proliferation and adult cardiomyocyte cell-cycle re-entry2014 · 73 citations
  5. 5Granulocyte colony-stimulating factor treatment plus dipeptidylpeptidase-IV inhibition augments myocardial regeneration in mice expressing cyclin D2 in adult cardiomyocytes2011 · 33 citations