Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
October 9, 2025Circulation Research

Abstract Thu014: Checkpoint kinase-2 regulates cardiomyocyte cell cycle and ameliorates cardiac function after myocardial infarction

View Full Paper
Ask AI
Bookmark
Share

Key result

Myocardial CHK2 suppression using AAV9-TnT-CHK2shRNA enhanced post-MI cardiac function, attenuated fibrosis, and promoted endogenous cardiomyocyte proliferation in mice at 1 week.

Population

mTmG lineage tracing mice with myocardial infarction induced by mid-LAD ligation

Comparison

AAV9-TnT-CHK2shRNA injected 1-day… vs Sham or untreated myocardial infarction

Design

Preclinical

Follow-up

1 week

Authors

DDDao‐Fu DaiJohns Hopkins UniversityCGChad E. GrueterUniversity of IowaNDNastaran DaneshgarUniversity of Iowa

Discussion

Loading...

Member takes

Implication

Suppression of checkpoint kinase 2 (CHK2) in cardiomyocytes promotes endogenous proliferation and improves cardiac function and remodeling after myocardial infarction in a mouse model.

Key Points

  • CHK2 suppression significantly improves cardiac function and reduces adverse remodeling after myocardial infarction.
  • Spatial transcriptomic analysis revealed enhanced mitochondrial and calcium handling gene expression in treated hearts.
  • Increased cardiomyocyte proliferation markers were noted, indicating effective recovery and regeneration after insult.
  • The findings suggest a shift towards a more favorable microenvironment for cardiomyocyte survival and function.

Structured PICO

P
Population
mTmG lineage tracing mice subjected to myocardial infarction and followed for 1 week.
I
Intervention
AAV9-TnT-CHK2shRNA injected 1-day post-myocardial infarction
C
Comparator
Sham or untreated myocardial infarction
O
Outcome
Cardiac function, scar size, and cardiomyocyte proliferation at 1 week after myocardial infarctionsurrogate

Suppression of checkpoint kinase 2 (CHK2) in cardiomyocytes promotes endogenous proliferation and improves cardiac function and remodeling after myocardial infarction in a mouse model.

Cite This Study

Dai et al. (2025) studied Myocardial infarction. AAV9-TnT-CHK2shRNA vs. Sham or untreated post-MI was evaluated on Cardiac function, scar size, and cardiomyocyte proliferation. Myocardial CHK2 suppression using AAV9-TnT-CHK2shRNA enhanced post-MI cardiac function, attenuated fibrosis, and promoted endogenous cardiomyocyte proliferation in mice at 1 week.

synapsesocial.com/papers/68e77f09d1c187e1c108fbd5https://doi.org/10.1161/res.137.suppl_1.thu014
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Cardiomyocyte cell cycle activation improves cardiac function after myocardial infarction2007 · 134 citations
  2. 2Checkpoint Kinase 1 Stimulates Endogenous Cardiomyocyte Renewal and Cardiac Repair by Binding to Pyruvate Kinase Isoform M2 C‐Domain and Activating Cardiac Metabolic Reprogramming in a Porcine Model of Myocardial Ischemia/Reperfusion Injury2024 · 12 citations
  3. 3Abstract Thu031: <i>MCM2</i> overexpression in the adult heart promotes cardiac rejuvenation and protection after infarction.2025
  4. 4Selective cardiomyocyte loss triggers myocardial regeneration via miR221 driven activation of cardiac stem cells and p57 suppression2026
  5. 5<i>MCM2</i> mediates post-MI cardioprotection by promoting the pro-angiogenic cardiosome signaling2024 · 1 citations