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Intermedin1-53 Ameliorates Homocysteine-Promoted Atherosclerotic Calcification by Inhibiting Endoplasmic Reticulum

Jin-Ling Ren1,2,3, Yue-Long Hou1,2,3, Xian-Qiang Ni1,2,3

  • 1Laboratory of Cardiovascular Bioactive Molecule, School of Basic Medical Sciences, Peking University, Beijing, China.

Journal of Cardiovascular Pharmacology and Therapeutics
|November 9, 2019
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Intermedin-1-53 peptide prevents atherosclerotic calcification in mice by reducing endoplasmic reticulum stress. This finding offers potential therapeutic strategies for cardiovascular disease.

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atherosclerotic calcificationendoplasmic reticulum stressintermedin

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Area of Science:

  • Cardiovascular Biology
  • Vascular Biology
  • Biomedical Research

Background:

  • Vascular calcification (VC) is a significant predictor of cardiovascular morbidity and mortality.
  • Intermedin-1-53 (IMD) is a peptide with known cardiovascular protective effects, including inhibition of vascular medial calcification.

Purpose of the Study:

  • To investigate the effects of IMD on atherosclerotic calcification induced by a high-fat diet and homocysteine (Hcy).
  • To elucidate the underlying mechanisms by which IMD influences atherosclerotic calcification.

Main Methods:

  • Atherosclerotic calcification was induced in ApoE-/- mice using a high-fat diet and Hcy in drinking water.
  • In vitro studies utilized human aorta vascular smooth muscle cells (HA-VSMCs) and primary rat VSMCs.
  • Endoplasmic reticulum stress (ERS) activation, osteogenic markers, and inflammatory cytokines were assessed.

Main Results:

  • Hcy treatment significantly increased atherosclerotic lesion areas and calcified nodules, which were reduced by IMD.
  • In vitro, Hcy increased alkaline phosphatase activity and calcium content in HA-VSMCs, effects blocked by IMD.
  • IMD alleviated endoplasmic reticulum stress (ERS) activation and reduced osteogenic and inflammatory markers.

Conclusions:

  • Intermedin-1-53 protects against Hcy-promoted atherosclerotic calcification in ApoE-/- mice.
  • The protective mechanism involves the inhibition of endoplasmic reticulum stress (ERS).