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Caspases01:24

Caspases

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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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Butachlor-Induced BAZ2B Activation Promotes Cardiomyocyte Senescence through cGAS-STING pathway.

Ming Lou1, Yi-Feng Huang1, Xin Su1

  • 1College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, P.R. China.

Journal of Agricultural and Food Chemistry
|March 13, 2026
PubMed
Summary
This summary is machine-generated.

This study reveals how the herbicide Butachlor causes heart damage by impairing mitochondria and cell growth. Targeting the BAZ2B protein and cGAS-STING pathway may prevent this herbicide-induced cardiotoxicity.

Keywords:
BAZ2BButachlorCardiotoxicitySenescencecGAS-STING

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Area of Science:

  • Environmental toxicology
  • Molecular biology
  • Cardiovascular research

Background:

  • Herbicides like Butachlor are essential in agriculture but pose health risks.
  • Butachlor (But) overuse can lead to environmental and health issues.
  • BAZ2B protein impacts cell proliferation and mitochondrial function.

Purpose of the Study:

  • To investigate the molecular mechanisms of Butachlor-induced cardiotoxicity.
  • To explore the role of BAZ2B in Butachlor-induced heart damage.

Main Methods:

  • Examined effects of Butachlor on cardiomyocyte structure and mitochondrial function.
  • Assessed impact on mitochondrial biogenesis, stress, and unfolded protein response.
  • Investigated Butachlor's influence on cell proliferation, senescence, BAZ2B expression, and the cGAS-STING pathway.

Main Results:

  • Butachlor induced cardiomyocyte structural injury and mitochondrial impairment.
  • Inhibition of mitochondrial biogenesis and induction of mitochondrial stress and unfolded protein response were observed.
  • Butachlor accelerated cellular senescence, upregulated BAZ2B, and activated the cGAS-STING pathway.

Conclusions:

  • Butachlor causes cardiotoxicity through mitochondrial dysfunction and cellular senescence.
  • The BAZ2B protein and cGAS-STING pathway are key mediators in herbicide-induced cardiotoxicity.
  • Modulating the BAZ2B-mediated cGAS-STING pathway offers a potential therapeutic strategy for preventing Butachlor cardiotoxicity.