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Related Experiment Video

Updated: May 10, 2025

Proteomics to Identify Proteins Interacting with P2X2 Ligand-Gated Cation Channels

Proteomics to Identify Proteins Interacting with P2X2 Ligand-Gated Cation Channels

Published on: May 18, 2009

P2X₇ Receptor Facilitates Cardiomyocyte Autophagy After Myocardial Infarction via Nox4/PERK/ATF4 Signaling Pathway.

Shuhong Zhang^1,2,3, Yingying Bi^1,2,3, Kaili Xiang^1,2,3

¹Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.

Cell Biochemistry and Function

|April 28, 2025

Summary

This summary is machine-generated.

Myocardial infarction (MI) triggers extracellular ATP release, activating P2X7 receptors. This exacerbates heart injury by promoting excessive autophagy via the Nox4/PERK/ATF4 pathway.

Keywords:

Nox4 P2X7 receptor autophagy myocardial infarction transcriptome sequencing

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Real-time Live-cell Flow Cytometry to Investigate Calcium Influx, Pore Formation, and Phagocytosis by P2X7 Receptors in Adult Neural Progenitor Cells

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Measuring Nucleotide Binding to Intact, Functional Membrane Proteins in Real Time

Measuring Nucleotide Binding to Intact, Functional Membrane Proteins in Real Time

Published on: March 11, 2021

Area of Science:

Cardiovascular Research
Cellular Signaling
Molecular Biology

Background:

Myocardial infarction (MI) is a leading cause of mortality, involving cellular damage and ATP release.
Extracellular ATP activates P2X7 receptors, initiating signaling cascades relevant to injury.
P2X7 receptor activation and autophagy are implicated in post-MI cardiac dysfunction.

Purpose of the Study:

To investigate the role of P2X7 receptors in myocardial infarction.
To elucidate the signaling pathways involved in hypoxia-induced autophagy post-MI.
To determine the contribution of Nox4 to P2X7-mediated cardiac injury.

Main Methods:

In vivo studies in a myocardial infarction model.
Transcriptome sequencing of infarcted myocardial tissue.
In vitro experiments using cardiomyocytes under hypoxic conditions.
Pharmacological inhibition of P2X7 receptors using A740003.
Assessment of autophagy-related proteins and Nox4 expression.

Main Results:

P2X7 receptor and autophagy-related protein levels were upregulated in the infarcted border zone.
Nox4 expression was increased post-MI, and A740003 reduced Nox4 and autophagy markers.
Hypoxia induced Nox4, PERK, ATF4, Beclin-1, and ATG5 in cardiomyocytes; A740003 inhibited these, but Nox4 overexpression counteracted this.
P2X7 receptor activation contributes to excessive autophagy via the Nox4/PERK/ATF4 pathway.

Conclusions:

P2X7 receptor is upregulated in MI and contributes to excessive cardiomyocyte autophagy.
The Nox4/PERK/ATF4 pathway mediates P2X7 receptor-induced autophagy and exacerbates MI injury.
Targeting the P2X7 receptor or its downstream pathways may offer therapeutic strategies for MI.