Perspectives in Understanding the Role of Human 17β-Hydroxysteroid Dehydrogenases in Health and Disease

Authors

  • Marc Meier,

    1. Helmholtz Zentrum München, German Research Center for Environmental Health, Institute of Experimental Genetics, Genome Analysis Center, Neuherberg, Germany
    Search for more papers by this author
  • Gabriele Möller,

    1. Helmholtz Zentrum München, German Research Center for Environmental Health, Institute of Experimental Genetics, Genome Analysis Center, Neuherberg, Germany
    Search for more papers by this author
  • Jerzy Adamski

    1. Helmholtz Zentrum München, German Research Center for Environmental Health, Institute of Experimental Genetics, Genome Analysis Center, Neuherberg, Germany
    Search for more papers by this author

Address for correspondence: Jerzy Adamski, Helmholtz Zentrum München, German Research Center for Environmental Health, Institute of Experimental Genetics, Genome Analysis Center, 85764 Neuherberg, Germany. Voice: +49-89-3187-3155; fax: +49-89-3187-3225. adamski@helmholtz-muenchen.de

Abstract

Steroid signaling involves specific receptors that mediate genomic effects and many further proteins responsible for fast nongenomic activities. Metabolism at the position 17 of the steroid scaffold plays a pivotal role in the final regulation of the biological potency of steroid hormones. Enzymes responsible for that, the 17β-hydroxysteroid dehydrogenases (17β-HSD), act as carbonyl reductases and require cofactors for their catalytic activity. There is a substantial amount of evidence that human 17β-HSDs are as well involved in the metabolic pathways of retinoids and fatty acid beyond that which has so far been anticipated. At present fourteen 17β-HSDs have been annotated and characterized, and more might follow. Many of 17β-HSDs have been shown to be involved in the pathogenesis of human disorders and are targets for therapeutic intervention. Strategies on deciphering the physiological role of the 17β-HSD and the genetic predisposition for associated diseases will be presented involving analyses of animal models.

Ancillary