Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
September 8, 2026International Journal of Molecular SciencesOpen Access

Elevated NEAT1 drives early post-MI ion channel remodeling, presenting a potential target against malignant arrhythmias.

View Full Paper
Ask AI
Bookmark
Share

Population

Post-MI human hearts (single-nucleus transcriptomic data) and hypoxic rat cardiomyocytes

Comparison

siRNA-mediated knockdown of NEAT1 vs Control (implied for siRNA knockdown)

Design

Preclinical

Key result

Elevated NEAT1 in the early myocardial infarction border zone drives ion channel remodeling by upregulating CACNA1C and PDLIM5, suggesting a potential target for preventing malignant arrhythmias.

Authors

JZJiuxiao ZhaoQZQian ZhuYLYang Lou

Discussion

Loading...

Member takes

Overview

Hypothesis-generating for NEAT1 as arrhythmia target post-MI; leaves open clinical relevance beyond hypoxic rat cardiomyocytes.

Key Points

  • To characterize cell-type-specific molecular mechanisms driving arrhythmogenic ion channel remodeling in border-zone cardiomyocytes during early myocardial infarction.
  • Integrated single-nucleus and spatial transcriptomics from human post-infarction heart tissue with gene co-expression and competing endogenous RNA network analyses.
  • Assessed regulatory interactions in vitro using hypoxic rat cardiomyocytes and siRNA-mediated knockdown of NEAT1.
  • Identified an arrhythmia-potential cardiomyocyte subpopulation in the infarct border zone defined by severe ion channel remodeling.
  • Demonstrated that NEAT1, CACNA1C, and PDLIM5 are concurrently upregulated under hypoxia, with NEAT1 silencing directly decreasing CACNA1C and PDLIM5 expression via a miR-204-5p/211-5p axis.

Structured PICO

P
Population
Post-MI human hearts (single-nucleus transcriptomic data) and hypoxic rat cardiomyocytes
E
Exposure
siRNA-mediated knockdown of NEAT1
C
Comparator
Control (implied for siRNA knockdown)
O
Outcome
Expression levels of CACNA1C and PDLIM5surrogate

Elevated NEAT1 in the early MI border zone drives ion channel remodeling, suggesting it as a potential therapeutic target to prevent post-MI malignant arrhythmias.

Cite This Study

Zhao et al. (2026) studied Early-stage myocardial infarction. Elevated NEAT1 was evaluated on Ion channel remodeling and gene expression. Elevated NEAT1 in the early myocardial infarction border zone drives ion channel remodeling by upregulating CACNA1C and PDLIM5, suggesting a potential target for preventing malignant arrhythmias.

synapsesocial.com/papers/6a9fd83b58e84d0ff5b47907https://doi.org/10.3390/ijms27177945
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. 1NMDA‐Type Glutamate Receptor Activation Promotes Ischemic Arrhythmias by Targeting the AKT1–TBX3–Nav1.5 Axis2025
  2. 2Abstract Wed010: Endothelial NFATc3 improved angiogenesis after myocardial infarction by upregulating lncRNA MALAT1 to promote mitochondrial function2025
  3. 3Single-cell transcriptomics and machine learning reveal RNF144B and C5AR1 as immune-related biomarkers and therapeutic targets in myocardial infarction2025
  4. 4Abstract Thu021: Regulatory Role of Non-Coding RNAs in Cardiomyocyte Cell Cycle Arrest and Postnatal Maturation2025
  5. 5Elektra-Qki and Alien-Wt1 lncRNA-protein interaction controls myocardial ion channel expression and epicardial EMT during heart development in mice2026