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INNOSC Theranostics and
            Pharmacological Sciences                                             AMPK in metabolism, energy and aging




            Table 2. (Continued)
            Compound                      Chemical structure           AMPK activation mechanism     References
            Nootkatone                                          Not specified                           68


            Thienopyridone (A-769662)                           Allosteric activator (AMPK binding, β1 subunit)  69







            Benzimidazole (Compound 911)                        Allosteric activator (AMPK binding, β1 subunit)  5




            Compound 991                                        Not specified (AMPK binding, β1 subunit)  70



            Compound-13                                         Allosteric activator (AMPK binding, α1 subunit)  71





            PT-1                                                Allosteric activator (AMPK binding, γ1 subunit)  72







            MT 63-78                                            Allosteric activator (AMPK binding, β1 subunit)  73






            R118                                                Respiratory chain blockage              69



            Abbreviations: AICAR: 5-Aminoimidazole-4-carboxamide ribonucleoside; ZMP: 5-Aminoimidazole-4-carboxamide-1-β-D-ribofuranosyl-5′-monophosphate;
            AMPK: 5' adenosine monophosphate-activated protein kinase; EGCG: Epigallocatechin-3-gallate; LKB1: Liver kinase B1;
            CaMKK: Calcium-calmodulin-dependent protein kinase; ROS: Reactive oxidative species; AMP: Adenosine monophosphate; ATP: Adenosine
            triphosphate.

            nigra pars compacta (SNpc), a region involved in the   remain  unclear.  However,  the  appearance  of  swollen  and
            development of specific symptoms.  However, long-  fragmented mitochondria has been reported across all
                                           84
            term treatment has been shown to negatively influence   species studied, suggesting that mitochondrial fragmentation
            intellectual capacities, with the exact mechanism remaining   is a senescence-promoting factor. 88-90
            unknown, though interference with vitamin B  absorption
                                                12
            is a likely factor. 85-87  Mitochondrial dynamics regulate   AMPK,  as  a  regulator  of  energy  homeostasis,  links
            many key cellular functions, including metabolic plasticity,   energy levels with the rate of aging and can be considered a
            mitochondrial turnover, and organelle communication,   modulator of senescence and lifespan extension, particularly
            but the mechanisms by which these functions are affected   through mechanisms such as caloric restriction (activated
            by perturbations of mitochondrial dynamics during aging   with a 30 – 70% reduction in the initial amount nutrient


             Volume 8 Issue 2 (2025)                        7                                doi: 10.36922/itps.4852
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