Related Experiment Video

Updated: Sep 16, 2025

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum
06:12

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Published on: May 3, 2024

2.3K

The m6A methyltransferase METTL14 governs NLRP3 and facilitates myocardial infarction via pyroptosis

Xiaoling Li1, Longwei Zhou1, Chengyan Yang1

  • 1Department of Critical Care Medicine, Guilin People's Hospital, Guilin, Guangxi, China.

Clinical Hemorheology and Microcirculation
|July 8, 2025
PubMed

Insights

METTL14 depletion inhibits N6-methyladenosine (m6A) methylation-driven pyroptosis in cardiomyocytes, reducing myocardial infarction injury. This suggests METTL14 is a potential therapeutic target for myocardial infarction.

Area of Science:

  • Cardiovascular Biology
  • Epigenetics
  • Molecular Medicine

Background:

  • N6-methyladenosine (m6A) methylation is implicated in myocardial infarction and cardiomyocyte pyroptosis.
  • METTL14, an m6A methyltransferase, is investigated for its role in these processes.

Purpose of the Study:

  • To explore the effects of METTL14 on cardiomyocyte pyroptosis and myocardial infarction.
  • To elucidate the underlying molecular mechanisms involving m6A methylation of NLRP3.

Main Methods:

  • In vivo studies utilized TTC staining, biochemical assays, and H&E staining.
  • In vitro pyroptosis was assessed via PI staining, immunofluorescence, and western blotting.
  • NLRP3 m6A methylation was analyzed using RIP, luciferase assays, Me-RIP, and mRNA stability tests.

Main Results:

  • METTL14 expression was elevated in myocardial infarction models and OGD-induced cardiomyocytes.
  • METTL14 depletion suppressed pyroptosis and myocardial injury.
  • METTL14 promoted NLRP3 mRNA stability via m6A methylation, and NLRP3 overexpression reversed these effects.

Conclusions:

  • METTL14 knockdown mitigates cardiomyocyte pyroptosis and myocardial infarction by reducing NLRP3 m6A methylation.
  • METTL14 presents a promising therapeutic target for myocardial infarction treatment.
Keywords:
METTL14NLRP3m6A methylationmyocardial infarctionpyroptosis

More Related Videos

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages06:52

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

Published on: May 21, 2018

10.9K
Evaluation of Caspase Activation to Assess Innate Immune Cell Death10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

3.4K

Related Concept Videos

Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
3.6K
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
4.9K