GDF11
[14] GDF11 belongs to the transforming growth factor beta superfamily that controls anterior-posterior patterning by regulating the expression of Hox genes.Administration of GDF11 in aged mice stimulates neuronal autophagy which improves memory and alleviates senescence and depression-like symptoms in a neurogenesis-independent manner.Tumor microenvironments often have low oxygen levels and increased inflammation, which could be the cause higher GDF11 expression in colon cancer patients..[27] In 2014, GDF11 was described as a life extension factor in two publications based on the results of parabiosis experiments in mice [28][29] that were chosen as Science's scientific breakthrough of the year.GDF11 induces generation of antioxidant enzymes (CAT, SOD and GPX), which directly results in reduction of ROS levels, which then decelerates protein oxidation, lipid peroxidation and possibly LF and SA-β-Gal development, which in turn extends lifespan of aged mice.[38] GDF11 triggers a calorie restriction‐like phenotype without affecting appetite or GDF15 levels in the blood, restores the insulin/IGF‐1 signaling pathway, and stimulates adiponectin secretion from white adipose tissue by direct action on adipocytes, while repairing neurogenesis in the aged brain.[40] GDF11 contributes to limiting functional damage of mitochondria in cardiomyocytes (heart cells) following ischemic (lack of blood flow) injury or anoxia (oxygen deprivation) insult, and repressing apoptosis in mitochondria-dependent and mitochondria-independent manners by increasing telomerase activities.Supplementing GDF11 increased tubular cell dedifferentiation and proliferation as well as improved the prognosis of old mice that underwent ischemia–reperfusion injury by upregulating the ERK1/2 signaling pathway.As the key member of the TGF-Beta superfamily, GDF11 represents a promising therapeutic agent for the treatment of a number of inflammatory skin diseases, including psoriasis.[47] This GDF11 paper summarizes GDF11 expression in various organs as well as a table showing effects of GDF11 in cardiac, muscle skeletal and nervous system disease.[28] Treatment of old mice to restore GDF11 to youthful levels recapitulated the effects of parabiosis and reversed age-related hypertrophy, revealing a therapeutic opportunity for cardiac aging.