Unveiling the Therapeutic Potential of KATP Channels in Parkinson's Disease: Exploring the Impact of Blockers and Inhibitors on Disease Progression and Treatment Outcomes

Parkinson's disease is a progressive neurodegenerative disorder marked by the degradation of dopaminergic neurons in the substantia nigra pars compacta. Several pathophysiological mechanisms contribute to it, including diminished mitochondrial function, heightened oxidative stress, and neuroinflammatory responses. Thus, researchers have recognized the importance of ATP-sensitive potassium channels (KATP) as essential regulators of neurotransmission, energy balance, and cell viability. The channels have variable functions in protecting neurons from oxidative damage, controlling neurotransmitter release, and affecting mitochondrial function. Dopaminergic neurons exhibit differential expression and regulation of KATP channels, suggesting selective neuronal vulnerability. The glibenclamide blocker and the diazoxide and Iptakalim activators can also help PD animal models' neuronal survival and function. However, their impact on disease progression and control of symptoms might vary under different circumstances. This review focuses on the importance of KATP channels in PD. It reviews innovative strategies that target these KATP channels to prevent neuronal loss and improve clinical symptoms.