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These senescent cells release harmful pro-inflammatory signals, known as the senescence-associated secretory phenotype (SASP), that damage surrounding tissues and disrupt overall organ function

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In the failing heart, increased levels of GPCR kinases (GRKs) phosphorylate, and thereby desensitize and downregulate, -ARs, resulting in a loss of cardiomyocyte contractile reserve

In the absence of the antioxidant potential of EGT, GSH must be diverted from gliotoxin biosynthesis, resulting in reduced levels of gliotoxin

Linus Pauling Institute Oregon State University Reviewed in February 2012 by: Suzanne Pilkington, Ph.D