Editorials |
From the Gaubius Laboratory, TNO-PG, The Netherlands.
Corresponding to Cornelis Kluft, Gaubius Laboratory, TNO-PG, Zernikedreef 9, 2333 CK Leiden, The Netherlands. E-mail c.kluft@pg.tno.nl
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The role of inflammation in cardiovascular disease has gained enormous interest in recent years, to a significant extent as a consequence of the ease with which the acute phase protein C-reactive protein (CRP) can be assessed as a marker of inflammation. More recently, CRP has not only to be considered a marker, but also a potential participant in the pathogenesis of cardiovascular disease, and various roles in cellular activation and in inflammatory processes have been proposed.1
See page 2063
Very recently, it has become firmly established that a genetic component exists for CRP. Baseline levels of CRP show a clear heritability of 40%2 and 39%3 in family studies. In twin studies, MacGregor et al4 observed 26% heritability in middle-aged twins; de Maat et al (unpublished data, 2003) observed heritability of 37% in male and 19% in female elderly twins; Hengstenberg et al5 found in families with myocardial infarction 31% related to genetic factors.
In this issues article by Brull et al,6 the involvement of genetics with CRP is further elucidated, not only the role of genetic variation in the CRP gene itself for baseline levels, but in particular the fact that the response to stimuli is linked to genetic variability in the CRP gene.
Genetic research on CRP can add to knowledge about the mechanisms of involvement of CRP in disease processes and may affect the use of CRP as a marker. It is of significance now to discuss important possible lessons we can learn from the genetic approach and
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