Molecular Variation Responsible for Cardiovascular Disease in Older Women - European Medical Journal

Molecular Variation Responsible for Cardiovascular Disease in Older Women

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VARIATIONS at a molecular level between men and women have been identified as a potential reason for the differences observed in the age of cardiovascular disease diagnosis between males and females. A study of healthy hearts from people of different age categories, conducted to identify differences between the sexes in mitochondrial function and inflammation during ageing, identified differences in SIRT1 levels, expression of superoxide dismutase 2, and the expression of catalase.

Heart tissue was collected from seven men and seven women aged 17–40 years and eight women and nine men aged 50–68 years. Levels of proteins involved in inflammation and the function of mitochondria were measured. The results showed that levels of SIRT1, a protein important for mitochondrial function, were higher in young women compared to young men; however, in older heart tissue, SIRT1 levels had only decreased in women. Similar results were found for the expression of superoxide dismutase, an antioxidant protein in the mitochondria, and catalase, an enzyme that protects cells from oxidative damage, both of which were higher in younger women compared to younger men, but the difference was lost in older heart tissue. In addition, compared with young men, young women were found to have higher levels of anti-inflammatory cytokines, but this difference diminished with age, suggesting that female hearts progress from an anti-inflammatory to a proinflammatory environment with age.

It is thought these differences may be linked to the reduction of oestrogen levels during and after the menopause; however, the mechanism by which this occurs is unclear. Dr Maria Luisa Barcena De Arellano, Institute of Gender Medicine, Charité University Medicine Berlin, Berlin, Germany, postulated: “We have previously shown that oestrogen improves the expression of mitochondrial proteins and antioxidant proteins and decreases oxidative stress. We think that the fall in oestrogen with menopause contributes to mitochondrial dysfunction.” Hormone replacement therapy to counteract the reduction of oestrogen during menopause is available to prevent the risk of heart disease but is not a suitable treatment for all women.

Being aware of these genetic variants and their link to cardiovascular disease will no doubt allow further research into new treatments to counteract these age-specific changes. Commenting on the future implications of the study, Dr De Arellano said: “Our study suggests that a new drug could be developed which increases the expression of mitochondrial proteins. This could improve mitochondrial function, reduce inflammation, and help to prevent cardiovascular disease in older women.”

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