Macrophages are vital cells in innate immunity and are a source of anti- and proinflammatory cytokines. Classical activators of macrophages include PAMP, LPS, or IFN-γ, but these cells can also respond to endogenous damage signals and stress. In response to DAMP (damage-associated molecular patterns), macrophages undergo physiological changes that lead to the production of proinflammatory cytokines and high levels of nitric oxide (NO) in a process known as polarization [30]. The polarization of macrophages has been widely studied and its role has gained prominence in several pathologies ranging from cancer to cardiovascular diseases [30]. Macrophage phenotypes can be grouped into two large families according to their characteristics and activation, including M1 macrophages (classic activation) and M2 macrophages (alternative activation) [30]. It has been shown in [31] that the presence of macrophages with these phenotypes in atherosclerotic plaques with M1 are considered to be atherogenic and have proinflammatory properties, while M2 appears to have a role in remodeling and healing, along with anti-inflammatory activity. Biochemically, the M1 macrophage mainly differs from M2 in arginine metabolism with the L-arginine/arginase pathway being primarily active, and the metabolism of l-arginine by NOS2 occurring only when it is stimulated [30].