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C1q/TNF-related protein-9 attenuates atherosclerosis through AMPK-NLRP3 inflammasome singling pathway

Hui Zhang1, Xinyang Gong1, Shimao Ni1

  • 1Department of Cardiology, Yiwu Central Hospital, No. 699 Jiangdong Road, Yiwu 322000, PR China.

International Immunopharmacology
|November 16, 2019
PubMed

Insights

C1q tumor necrosis factor-related protein 9 (CTRP9) protects against atherosclerosis by inhibiting the NLRP3 inflammasome via the Adenosine Monophosphate Activated Protein Kinase (AMPK) pathway. This CTRP9-AMPK-NLRP3 inflammasome pathway was validated in a mouse model.

Area of Science:

  • Cardiovascular Research
  • Inflammation Biology
  • Metabolic Disease

Background:

  • C1q tumor necrosis factor-related protein 9 (CTRP9) may protect against atherosclerosis by influencing inflammation and cell function through the Adenosine Monophosphate Activated Protein Kinase (AMPK) pathway.
  • The NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome is implicated in atherosclerosis development and regulated by AMPK.
  • The precise role of CTRP9 in modulating NLRP3 inflammasome activity during atherosclerosis remains to be elucidated.

Purpose of the Study:

  • To investigate the effect of CTRP9 on NLRP3 inflammasome activation in atherosclerosis.
  • To elucidate the involvement of the AMPK pathway in the CTRP9-mediated regulation of the NLRP3 inflammasome.
  • To validate the CTRP9-AMPK-NLRP3 inflammasome pathway in a preclinical atherosclerosis model.

Main Methods:

  • Macrophage cells were treated with oxidized low-density lipoprotein (ox-LDL) and CTRP9.
  • NLRP3 inflammasome activation was assessed by measuring IL-1β and caspase-1 p10 release via ELISA and western blot.
  • AMPK inhibition and atherosclerosis mouse models were used to validate the pathway.

Main Results:

  • CTRP9 suppressed NLRP3 protein expression and inflammasome activity in ox-LDL-stimulated macrophages.
  • AMPK inhibition reversed the suppressive effects of CTRP9 on NLRP3 inflammasome activity.
  • CTRP9 administration reduced atherosclerosis development in mice, an effect abolished by AMPK inhibition.

Conclusions:

  • CTRP9 exhibits atheroprotective effects.
  • The CTRP9 exerts its atheroprotective function through the CTRP9-AMPK-NLRP3 inflammasome pathway.
  • Targeting the CTRP9-AMPK-NLRP3 inflammasome axis may represent a novel therapeutic strategy for atherosclerosis.
Abstract

Keywords:
AMPK, NLRP3AtherosclerosisC1q/TNF-related protein-9CTPR9

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