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Research paper| Volume 22, ISSUE 2, P215-227, September 01, 1975

Homocysteine theory of arteriosclerosis

  • Kilmer S. McCully
    Correspondence
    Address correspondence to Dr. Kilmer S. McCully, Department of Pathology, The Massachusetts General Hospital, Boston, Mass. 02114, U.S.A.
    Affiliations
    Department of Pathology, Harvard Medical School, the James Homer Wright Pathology Laboratories, Massachusetts General Hospital, Boston, Mass., USA

    Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, Mass., U.S.A.
    Search for articles by this author
  • Robert B. Wilson
    Footnotes
    Affiliations
    Department of Pathology, Harvard Medical School, the James Homer Wright Pathology Laboratories, Massachusetts General Hospital, Boston, Mass., USA

    Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, Mass., U.S.A.
    Search for articles by this author
  • Author Footnotes
    ∗ Present address: School of Veterinary Medicine, University of Missouri, 202 Connaway, Columbia, Mo. 65201, U.S.A.
DOI:https://doi.org/10.1016/0021-9150(75)90004-0
Homocysteine theory of arteriosclerosis
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      Abstract

      Arteriosclerotic plaques were found in the aorta and arteries of rabbits given homocysteine thiolactone, methionine or homocysteic acid, both parenterally and in a synthetic diet. Animals given large doses of parenteral methionine or homocysteine thiolactone died of pulmonary embolism and pulmonary infarct. Pyridoxine prevented thrombosis and pulmonary embolism but did not prevent arteriosclerotic plaques. These findings and previous work, showing a new metabolic pathway for sulfate ester synthesis from methionine, the somatotrophic activity of homocysteic acid, and control of cellular growth and intercellular matrix synthesis by homocysteine derivatives, suggest a theory to explain aspects of the pathogenesis of arteriosclerosis.

      Keywords

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      Article Info

      Publication History

      Accepted: April 15, 1975
      Received: May 13, 1974

      Footnotes

      ☆Supported by grants from the National Institutes of Health, AM-15978 and CDA-HL-18747, and the American Heart Association, 70-704 and 73-655.

      Identification

      DOI: https://doi.org/10.1016/0021-9150(75)90004-0

      Copyright

      © 1975 Published by Elsevier Inc.

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