M A Hofmann

Summary

Affiliation: Columbia University
Country: USA

Publications

  1. pmc Hyperhomocysteinemia enhances vascular inflammation and accelerates atherosclerosis in a murine model
    M A Hofmann
    College of Physicians and Surgeons, Columbia University, 630 W 168th Street, P and S 17 501, New York, NY 10032, USA
    J Clin Invest 107:675-83. 2001
  2. ncbi Receptor for advanced glycation end products mediates inflammation and enhanced expression of tissue factor in vasculature of diabetic apolipoprotein E-null mice
    T Kislinger
    College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    Arterioscler Thromb Vasc Biol 21:905-10. 2001
  3. ncbi RAGE and arthritis: the G82S polymorphism amplifies the inflammatory response
    M A Hofmann
    College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    Genes Immun 3:123-35. 2002
  4. ncbi RAGE is a multiligand receptor of the immunoglobulin superfamily: implications for homeostasis and chronic disease
    L G Bucciarelli
    College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    Cell Mol Life Sci 59:1117-28. 2002
  5. ncbi RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides
    M A Hofmann
    College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    Cell 97:889-901. 1999

Collaborators

Detail Information

Publications5

  1. pmc Hyperhomocysteinemia enhances vascular inflammation and accelerates atherosclerosis in a murine model
    M A Hofmann
    College of Physicians and Surgeons, Columbia University, 630 W 168th Street, P and S 17 501, New York, NY 10032, USA
    J Clin Invest 107:675-83. 2001
    ..These findings implicate HHcy in atherosclerotic plaque progression and stability, and they suggest that dietary enrichment in vitamins essential for the metabolism of HC may impart protective effects in the vasculature...
  2. ncbi Receptor for advanced glycation end products mediates inflammation and enhanced expression of tissue factor in vasculature of diabetic apolipoprotein E-null mice
    T Kislinger
    College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    Arterioscler Thromb Vasc Biol 21:905-10. 2001
    ..These data suggest that activation of RAGE primes cells targeted for perturbation in diabetic tissues by the induction of proinflammatory mediators...
  3. ncbi RAGE and arthritis: the G82S polymorphism amplifies the inflammatory response
    M A Hofmann
    College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    Genes Immun 3:123-35. 2002
    ..These data suggest that RAGE 82S upregulates the inflammatory response upon engagement of S100/calgranulins, and, thereby, may contribute to enhanced proinflammatory mechanisms in immune/inflammatory diseases...
  4. ncbi RAGE is a multiligand receptor of the immunoglobulin superfamily: implications for homeostasis and chronic disease
    L G Bucciarelli
    College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    Cell Mol Life Sci 59:1117-28. 2002
    ..Implications for the role of these ligands interacting with RAGE in homeostasis and disease will be considered...
  5. ncbi RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides
    M A Hofmann
    College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    Cell 97:889-901. 1999
    ..These data highlight a novel paradigm in inflammation and identify roles for EN-RAGEs and RAGE in chronic cellular activation and tissue injury...