Identification of a blood molecule that promotes aging-related phenotypes

Identification of a blood molecule that promotes aging-related phenotypes

a step toward possible prevention of aging-associated conditions

Jun 9, 2012

Under the leadership of KOMURO Issei , Professor, Department of Cardiovascular Medicine, Internal Medicine Course, Osaka University Graduate School of Medicine, a group of Osaka University researchers has succeeded in identifying a molecule in blood that promotes aging-related decline.
The group targeted identification of a molecule activating wnt/ß-catenin signaling in blood. A molecule in blood that binds with wnt receptors and modulates wnt/ß-catenin signals was found to be C1q, a molecule that also plays an important role in immune responses. The research group found that the level of C1q in the blood of old mice and mice suffering heart failure was higher than in younger mice.
This research clarified for the first time that complement C1q that had been thought to be related only to immunity was also related to aging. While noting that C1q decreased skeletal muscle regeneration in young mice (a phenomenon normally seen in older mice), the researchers noted that C1s and C1r reduced this aging-associated impairment (i.e., reduction of regenerative capacity of skeletal muscle) in older mice.

In this way, the research group demonstrated the possibility of preventing many aging-associated conditions through inhibition of the wnt/ß-catenin signal by C1q.
Under the leadership of Osaka University, supported by Grant-in-Aid for Scientific Research (S) from MEXT and the Core Research for Evolutionary Science and Technology (CREST), this research was conducted in cooperation with Chiba University, Hokkaido University, Imperial College London, U.K. and Boston University, USA.

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To learn more about this important discovery, please read the full research report entitled " Complement C1q Activates Canonical Wnt Signaling and Promotes Aging-Related Phenotypes " available at this page at the Cell Press website.

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