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FBXL10 regulates cardiac dysfunction in diabetic cardiomyopathy via the PKC β2 pathway

Leilei Yin1, Yingying Fang2, Tao Song1

  • 1Department of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.

Journal of Cellular and Molecular Medicine
|February 1, 2019
PubMed

Insights

FBXL10 protects against diabetic cardiomyopathy (DCM) by reducing inflammation and oxidative stress. Overexpression of FBXL10 preserves cardiac function in a rat model, suggesting therapeutic potential for DCM.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Endocrinology

Background:

  • Diabetic cardiomyopathy (DCM) involves cardiac tissue necrosis, fibrosis, and hypertrophy.
  • FBXL10's role in DCM is not well understood.

Purpose of the Study:

  • To investigate FBXL10's effect on DCM in a rat model.
  • To explore the mechanisms by which FBXL10 might attenuate DCM.

Main Methods:

  • Utilized a streptozotocin (STZ)-induced rat model of DCM.
  • Assessed FBXL10 expression and its effects on high glucose-induced cellular damage in vitro.
  • Examined the impact of cardiomyocyte-specific FBXL10 overexpression on cardiac function and signaling pathways.

Main Results:

  • FBXL10 expression was decreased in diabetic rat hearts.
  • FBXL10 mitigated high glucose-induced inflammation, oxidative stress, and apoptosis in vitro.
  • FBXL10 activated the PKC β2 signaling pathway.
  • FBXL10 overexpression attenuated oxidative stress, inflammation, and cardiomyocyte death, preserving cardiac function in STZ-induced DCM rats.

Conclusions:

  • FBXL10 demonstrates protective effects against DCM.
  • FBXL10 acts, in part, through the PKC β2 pathway.
  • FBXL10 holds therapeutic potential for treating diabetic cardiomyopathy.

Keywords:
ApoptosisDiabetic cardiomyopathyFBXL10InflammationPKC β2oxidative stress

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