Mitochondria-targeted agents: Future perspectives of mitochondrial pharmaceutics in cardiovascular diseases

Figure 1 Formation of various reactive oxygen species in mitochondria. HO.: Hydroxyl radical; O₂^.-: Super oxide anion radical; ONOO^-: Peroxynitrite; mtNOS: Mitochondrial-specific nitric oxide synthase; NO: Nitric oxide.

Figure 2 Factors that form and attenuate (antioxidants) reactive oxygen species in mitochondria. SDH: Succinate dehydrogenase; αKGDH: Alpha ketoglutarate dehydrogenase; MAO: Monoamine oxidase; Trx: Thioredoxins; Prx: Peroxiredoxin; OXPHOS: Oxidative phosphorylations; TNF-α: Tumor necrosis factor-alpha; GSH: Reduced glutathione; MnSOD: Manganese containing superoxide dismutase; GPx1: Glutathione peroxidase; CoQ₁₀: Co-enzyme Q₁₀.

Figure 3 Damage induced by reactive oxygen species in mitochondria. OXPHOS: Oxidative phosphorylations; ROS: Reactive oxygen species.

Figure 4 Crosstalk between mitochondrial Ca²⁺ handling and reactive oxygen species generation. PTP: Permeability transition pore; NOS: Nitric oxide synthase; ADP: Adenosine diphosphate; ATP: Adenosine triphosphate.

Figure 5 Myocardial infarction-induced mitochondrial damage and dysfunction that resulted in heart failure.