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These results indicate that the protective effects against oxidative injury are largely dependent on MAPKAPK2 expression

demonstrated that mice fed with a high-fat diet (HFD) and treated with L-NAME developed pulmonary congestion, diastolic dysfunction, cardiac hypertrophy with fibrosis, and exercise intolerance, whereas treatment with HFD or L-NAME alone only elicited a partial phenotype

K.GrabruckerA

Age-related reduction of mitochondrial function is accompanied by a decline in the mitochondrial capacity for ATP production by oxidative phosphorylation [62], a reduction in the NAD + pool [63] by consuming processes (PARP, CD38, and SIRT1) [64], and further an increase in ROS generation by an inefficient electron transport chain (ETC) [26]