Mouse models of human disease have made it possible to gain important insights into many conditions. However, many diseases remain for which no mouse model exists, and large proportion of human diseases without mouse models are associated with aging.
Researchers in Deepak Srivastava's laboratory at the Gladstone Institute of Cardiovascular Disease hypothesized that mice may be protected from age-associated human diseases due to the relatively longer length of their telomeres, the regions at the end of chromosomes that help guard against deterioration. In work published this week in the JCI, the researchers used mice with shortened telomeres to examine a genetic defect that causes an age-associated congenital heart disease in humans.
Although mice with normal telomeres did not develop heart disease, the researchers observed cardiac symptoms that were similar to the human heart condition in telomere-shortened mice. Moreover, in telomere-shortened mice, they observed that genes interacting with telomeres were dysregulated, suggesting that telomere length plays a role in regulating gene expression. Altogether, these findings indicate that decreasing telomere length may contribute to the onset of age-related diseases.
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