Peking University, Feb. 25, 2010: On February 20, "Klotho suppresses RIG-I-mediated senescence-associated inflammation" written by Gu Jun and his colleagues from the School of Life Sciences at Peking University was published in the journal Nature Cell Biology.

The research work done by Gu Jun et al. uncovered for the first time the mechanism in which klotho functions as an anti-ageing factor through the suppression of RIG-I(retinoic-acid-inducible gene-I)-mediated inflammation. Researchers have long since known that inflammation occurrs along with the senescence of cells and the body, but the mechanisms underlying the senescence-associated inflammation have been hitherto largely unknown.

In their research, Gu Jun et al. have found that RIG-I/MAVS(mitochondrial antiviral signaling) signaling mediates senescence and senescence-associated inflammation. In MAVS-deficient cells and mice, senescence and senescence-associated inflammation decline dramatically. In replicatively senescent cells, silencing of RIG-I can suppress the senescence-associated inflammation and slow the senescence process. Further research has found that the anti-ageing protein klotho is a suppression factor for RIG-I that can suppress RIG-I-mediated inflammation, and klotho-deficient mice show a significantly higher level of inflammation. In the meanwhile, their study has found that the expression of RIG-I increases while the expression of klotho decreases in the senescent process, which indicates senescence is an inflammatorily imbalanced natural procedure. In the process of senescence, cells and organism alike are gradually inclined towards inflammation, while the suppression of inflammation is gradually weakened, leading to the chronic senescence-associated inflammation. This explains why senescence as a natural phenomenon often accompanies inflammation.

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Klotho suppresses RIG-I-mediated senescence-associated inflammation

Translated by: Xu Xinyi
Edited by: Su Juan
Source: PKU News (Chinese)