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Related Experiment Video

Updated: Jun 13, 2026

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07:14

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Published on: July 13, 2018

Subthreshold Thermal Stress Aggravates Methamphetamine-Induced Cardiomyocyte Pyroptosis via the Mitochondrial

Mengmeng Wang1, Congcong Hou2, Menglian Hu2

  • 1Clinical Medical College, Hebei University, Baoding 071000, China.

International Journal of Molecular Sciences
|June 12, 2026
PubMed
Summary

Environmental heat stress worsens methamphetamine (METH) cardiotoxicity by damaging mitochondria and triggering cell death pathways. Targeting mitochondrial reactive oxygen species (ROS) with antioxidants like MitoQ may protect against METH-induced heart injury.

Keywords:
BCL2-associated Xcardiomyocyte pyroptosismethamphetaminemitochondria-targeted antioxidantmitochondrial DNAmitoquinonereactive oxygen speciessubthreshold thermal stress

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Published on: October 27, 2020

Area of Science:

  • Cardiovascular Toxicology
  • Environmental Health
  • Mitochondrial Biology

Background:

  • Methamphetamine (METH) abuse is a significant cause of cardiac injury and mortality.
  • Environmental factors, such as elevated ambient temperatures, can exacerbate METH-related cardiovascular risks.
  • The precise mechanisms linking environmental stressors to METH cardiotoxicity are not fully understood.

Purpose of the Study:

  • To investigate how subthreshold thermal stress (STS) influences METH-induced cardiomyocyte injury.
  • To elucidate the molecular pathways involved in the combined effects of METH and heat on cardiac cells.
  • To evaluate the therapeutic potential of targeting mitochondrial oxidative stress.

Main Methods:

  • In vivo studies exposed mice to METH under normothermic (22 °C) or STS (28 °C) conditions.
  • In vitro studies used H9c2 cardiomyocytes exposed to METH at 37 °C or 39 °C.
  • Assessed cardiac dysfunction, mitochondrial damage, oxidative stress, and key signaling molecules (BAX, mtDNA, NLRP3 inflammasome, caspase-1/Gasdermin D).

Main Results:

  • STS significantly potentiated METH-induced cardiac dysfunction, mitochondrial damage, and oxidative stress.
  • Co-exposure impaired mitochondrial respiratory chain complex I, increased mitochondrial ROS (mtROS), and activated the BAX/mtDNA/NLRP3 inflammasome axis, leading to pyroptosis.
  • Mitoquinone (MitoQ) treatment attenuated METH cardiotoxicity by scavenging mtROS and inhibiting downstream apoptotic and pyroptotic pathways.

Conclusions:

  • Subthreshold thermal stress exacerbates METH-induced cardiotoxicity through mitochondrial dysfunction and oxidative stress.
  • The BAX/mtDNA/NLRP3 inflammasome pathway is critical in mediating METH and heat-induced cardiomyocyte pyroptosis.
  • Mitochondrial redox modulation, specifically targeting mtROS, represents a promising therapeutic strategy for psychostimulant-associated cardiovascular injury.