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Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
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CTRP12 ameliorates atherosclerosis by promoting cholesterol efflux and inhibiting inflammatory response via the

Gang Wang1, Jiao-Jiao Chen2, Wen-Yi Deng2

  • 1Department of Cardiology, The First Affiliated Hospital of University of South China, Hengyang, 421001, Hunan, China.

Cell Death & Disease
|March 11, 2021
PubMed

Insights

C1q tumor necrosis factor-related protein 12 (CTRP12) protein reduces atherosclerosis by improving cholesterol transport and decreasing inflammation. CTRP12 may offer a new therapeutic strategy for cardiovascular disease.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Atherosclerosis Research

Background:

  • C1q tumor necrosis factor-related protein 12 (CTRP12), an adiponectin paralog, is linked to cardiovascular disease.
  • The specific role of CTRP12 in atherogenesis remains largely unexplored.

Purpose of the Study:

  • To investigate the impact of CTRP12 on atherosclerosis development.
  • To elucidate the molecular mechanisms underlying CTRP12's function in this process.

Main Methods:

  • In vitro studies using lipid-laden macrophages with lentivirus-mediated CTRP12 overexpression.
  • In vivo studies involving apolipoprotein E-deficient (apoE-/-) mice fed a Western diet and treated with CTRP12-expressing lentiviral vectors.
  • Analysis of lipid accumulation, inflammatory markers, cholesterol efflux, macrophage polarization, atherosclerotic lesion size, and plasma lipid profiles.

Main Results:

  • CTRP12 overexpression inhibited lipid accumulation and inflammation in macrophages.
  • CTRP12 decreased miR-155-5p and increased liver X receptor α (LXRα), promoting cholesterol efflux via ABCA1 and ABCG1.
  • In vivo, CTRP12 reduced atherosclerotic lesions, improved high-density lipoprotein cholesterol, enhanced reverse cholesterol transport, and decreased inflammation in apoE-/- mice.

Conclusions:

  • CTRP12 protects against atherosclerosis by enhancing reverse cholesterol transport and mitigating vascular inflammation through the miR-155-5p/LXRα pathway.
  • Augmenting CTRP12 levels presents a potential novel therapeutic avenue for atherosclerosis treatment.

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