Antimicrobial blue light (aBL, 400–470 nm) has emerged as a promising strategy for killing pathogenic microorganisms, including multidrug-resistant strains, due to its intrinsic photobiological properties. Unlike conventional photodynamic therapy, aBL does not require exogenous photosensitizers (PSs) to elicit phototoxicity; instead, it activates endogenous PSs naturally present in microorganisms, inducing cytotoxic effects primarily through photochemical mechanisms. The photochemical pathway involves the generation of reactive oxygen species (ROS), including singlet oxygen, superoxide anions, hydroxyl radicals, and hydrogen peroxide, which cause oxidative damage to microbial DNA, lipids, proteins, and metabolic pathways. Key endogenous PSs mediating these effects include tetrapyrrole-based compounds such as metal-free porphyrins (uroporphyrin III, coproporphyrin III, and protoporphyrin IX) and chlorophyll, as well as flavin derivatives like riboflavin, flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and lumichrome. While photochemical ROS generation is the primary antimicrobial mechanism of aBL, non-photochemical effects—such as membrane depolarization and disruption—have also been observed under specific conditions, such as pulsed illumination. This review delineates the specific endogenous PSs involved in both photochemical and non-photochemical mechanisms and highlights their structural and functional roles in mediating microbial susceptibility to aBL. Understanding these mechanisms provides insights into optimizing aBL parameters for clinical and environmental antimicrobial applications, offering a safe and targeted approach to combat pathogenic microorganisms.