https://www.selleckchem.com/products/cb-5083.html Ion exchange between intracellular and extracellular spaces is the basic mechanism for controlling cell metabolism and signal transduction. This process is mediated by ion channels and transporters on the plasma membrane, or intracellular membranes that surround various organelles, in response to environmental stimuli. Macroautophagy (hereafter referred to as autophagy) is one of the lysosomal-dependent degradation pathways that maintains homeostasis through the degradation and recycling of cellular components (e.g., dysfunctional proteins and damaged organelles). Although autophagy-related (ATG) proteins play a central role in regulating the formation of autophagy-related member structures (e.g., phagophores, autophagosomes, and autolysosomes), the autophagic process also involves changes in expression and function of ion channels and transporters. Here we discuss current knowledge of the mechanisms that regulate autophagy in mammalian cells, with special attention to the ion channels and transporters. We also highlight prospects for the development of drugs targeting ion channels and transporters in autophagy.Purpose To report a case of initial cone dystrophy that advanced to a cone-rod dystrophy with homozygous variants in the POC1B gene.Methods Retinal structure and visual function assessments were performed using fundoscopy, spectral-domain optical coherence tomography, full field electroretinography, semi-kinetic perimetry, and Ishihara plate testing. A DNA sample was collected and sent for diagnostic molecular genetic testing with a cone-rod dystrophy panel.Results Clinical examination and electroretinography confirmed a clinical diagnosis of cone dystrophy. Molecular genetic testing revealed homozygous variants in POC1B (c.1355 G > A, p.(Arg452Gln)). Follow-up three years later showed progression to a cone-rod dystrophy.Conclusion Our case describes an ophthalmological phenotype associated with a homozygous P