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Dysfunction of thioredoxin triggers inflammation through activation of autophagy in chicken cardiomyocytes

Jie Yang1, Yafan Gong1, Jingzeng Cai1

  • 1College of Veterinary Medicine, Northeast Agricultural University, Harbin, People's Republic of China.

Biofactors (Oxford, England)
|February 8, 2020
PubMed

Insights

Thioredoxin (Txn) deficiency in cardiomyocytes triggers autophagy and inflammation, leading to cell damage. This study clarifies the mechanism behind Txn

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cellular Biology

Background:

  • Thioredoxin (Txn) is a vital hydrogen carrier protein.
  • Txn deficiency is linked to cardiomyocyte injury, but the mechanism is unclear.

Purpose of the Study:

  • To elucidate the mechanistic response of cardiomyocytes to Thioredoxin (Txn) suppression.
  • To investigate the roles of autophagy and apoptosis in Txn-deficient cardiomyocytes.

Main Methods:

  • Established Txn dysfunction models using siRNA and PX-12 in cardiomyocytes.
  • Measured reactive oxygen species (ROS) levels, inflammation factors, and key autophagy/apoptosis proteins.
  • Utilized heatmap analysis for data interpretation.

Main Results:

  • Txn dysfunction elevated ROS release and activated autophagy by upregulating Beclin-1 and LC3.
  • Autophagy activation modulated inflammatory responses in cardiomyocytes.
  • Txn suppression inhibited apoptosis via Caspase-3 inhibition in chicken cardiomyocytes.

Conclusions:

  • Txn deficiency in chicken cardiomyocytes induces autophagy, leading to significant inflammatory reactions and subsequent cell damage.
  • Understanding this pathway is crucial for addressing cardiomyocyte injury related to Txn dysfunction.
Keywords:
apoptosisautophagycardiomyocyteschickenthioredoxin (Txn)

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