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Angiotensin-(1-7) ameliorates high glucose-induced vascular endothelial injury through suppressing chloride channel 3

Fei Cheng1,2, Jing Liu3, Zhuolin Guo2

  • 1Second Ward of Cardiovascular Medicine, Dongguan Songshan Lake Center Hospital, Affiliated Dongguan Shilong People's Hospital of Southern Medical University, Dongguan City, Guangdong Province, China.

Bioengineered
|January 31, 2022
PubMed

Insights

Angiotensin-(1-7) peptide protects against high glucose-induced vascular endothelial injury by downregulating chloride channel 3 (CIC-3). This finding suggests Angiotensin-(1-7) may be a therapeutic target for preventing diabetic cardiovascular disease.

Area of Science:

  • Cardiovascular Science
  • Endocrinology
  • Molecular Biology

Background:

  • Diabetes Mellitus (DM) significantly increases cardiovascular disease (CVD) risk, with limited therapeutic options for diabetic CVD.
  • Vascular endothelial injury is a critical factor in the development of diabetic CVD.
  • The protective role of Angiotensin-(1-7) (Ang-(1-7)) against diabetic CVD, specifically its effect on endothelial injury, requires further clarification.

Purpose of the Study:

  • To investigate whether Ang-(1-7) attenuates high glucose (HG)-induced vascular endothelial injury.
  • To elucidate the underlying molecular mechanisms, including the role of chloride channel 3 (CIC-3) and Mas receptor.

Main Methods:

  • Utilized bEnd3 cells exposed to high glucose (HG) conditions.
  • Assessed the effects of Ang-(1-7) on endothelial injury markers.
  • Investigated the expression and function of CIC-3 and its regulation by Ang-(1-7) via the Mas receptor.
  • Measured reactive oxygen species (ROS), nitric oxide (NO), and cytokine production.

Main Results:

  • Ang-(1-7) alleviated HG-induced endothelial injury in bEnd3 cells.
  • Ang-(1-7) downregulated HG-induced CIC-3 expression through the Mas receptor.
  • HG-induced CIC-3 increased ROS and cytokine production while decreasing NO levels.
  • Ang-(1-7) treatment reversed these effects by inhibiting CIC-3, thereby preserving ROS, NO, and cytokine balance.

Conclusions:

  • Ang-(1-7) mitigates HG-induced vascular endothelial injury by inhibiting CIC-3 via the Mas receptor.
  • This mechanism highlights Ang-(1-7) as a potential therapeutic strategy for diabetic CVD by targeting endothelial dysfunction.

Keywords:
Angiotensin-(1-7)Diabetes mellituscardiovascular diseasechloride channel 3vascular endothelial injury

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