On the other hand, the paracrine effects of GDF15 in non-senescent ECs showed that GDF15 increased proliferation, migration, and NO production and activated several signaling pathways such as AKT, ERK1/,2, and SMAD2 without triggering any oxidative stress, and therefore, preventing the endothelial dysfunction (Ha et al., 2019). This evidence concerns the gene GDF15 and endothelial dysfunction.