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Experimental study on alleviating atherosclerosis through intervention of mitochondrial calcium transport and calcium-induced membrane permeability transition
  1. Sisi Chen1,
  2. Jianing Wang1,2,
  3. Lei Zhang3,
  4. Hao Xia1,4,5
  1. 1 Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China
  2. 2 Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei, China
  3. 3 Department of Cardiology and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei, China
  4. 4 Cardiovascular Research Institute, Wuhan University, Wuhan, Hubei, China
  5. 5 Hubei Key Laboratory of Cardiology, Wuhan, Hubei, China
  1. Correspondence to Dr Hao Xia, Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; xiahao1966{at}163.com

Abstract

To investigate the effort of mitochondrial calcium transport and calcium-induced membrane permeability transition in alleviating atherosclerosis. The experimental mice were divided into three groups: the control group (C57BL/6 mice with normal diet), the atherosclerosis group (apolipoprotein E-deficient (ApoE−/−) mice with high-fat diet) and the mitochondrial targeting agent group (ApoE−/− mouse with high-fat diet). The mean fluorescence intensity of Ca2+ in the atherosclerosis group is significantly higher than control group and mitochondrial targeting agent group. But the mean fluorescence intensity of Ca2+-ATPase is lower than other groups. The macrophage recruitment (F4/80 positive area) and the expression of tumor necrosis factor alpha, interleukin-6, pyrin domain containing protein 3, intercellular cell adhesion molecule-1, p38 mitogen-activated protein kinase and Jun kinase 1/2 phosphorylation in the atherosclerosis group are higher that other groups. Treatment with mitochondrial targeting agents reduced the levels of elevated cyt C and cleaved caspase-3 in atherosclerotic mice (p<0.05). Mitochondrial targeting agents interfere with mitochondrial calcium transport and calcium-induced membrane permeability transition, inhibit MAPK/JNK pathway activation, inhibit foam cell formation and alleviate the process of atherosclerosis.

  • atherosclerosis
  • endothelial cells

Data availability statement

Data are available upon reasonable request.

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Data availability statement

Data are available upon reasonable request.

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Footnotes

  • Contributors SC, JW, LZ and HX contributed to the conception and design of the study; SC, JW and LZ performed the experiments, collected and analyzed data; SC and JW wrote the manuscript; all authors reviewed and approved the final version of the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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