Pathophysiological Roles of Ion Channels in Epidermal Cells, Immune Cells, and Sensory Neurons in Psoriasis
- Authors
- Kim, Hyungsup; Choi, Mi Ran; Jeon, Seong Ho; Jang, Yongwoo; Yang, Young Duk
- Issue Date
- 2024-03
- Publisher
- Multidisciplinary Digital Publishing Institute (MDPI)
- Citation
- International Journal of Molecular Sciences, v.25, no.5
- Abstract
- Psoriasis is a chronic inflammatory skin disease characterized by the rapid abnormal growth of skin cells in the epidermis, driven by an overactive immune system. Consequently, a complex interplay among epidermal cells, immune cells, and sensory neurons contributes to the development and progression of psoriasis. In these cellular contexts, various ion channels, such as acetylcholine receptors, TRP channels, Ca2+ release-activated channels, chloride channels, and potassium channels, each serve specific functions to maintain the homeostasis of the skin. The dysregulation of ion channels plays a major role in the pathophysiology of psoriasis, affecting various aspects of epidermal cells, immune responses, and sensory neuron signaling. Impaired function of ion channels can lead to altered calcium signaling, inflammation, proliferation, and sensory signaling, all of which are central features of psoriasis. This overview summarizes the pathophysiological roles of ion channels in epidermal cells, immune cells, and sensory neurons during early and late psoriatic processes, thereby contributing to a deeper understanding of ion channel involvement in the interplay of psoriasis and making a crucial advance toward more precise and personalized approaches for psoriasis treatment.
- Keywords
- CALCIUM-SENSING RECEPTOR; NICOTINIC ACETYLCHOLINE-RECEPTOR; ANOCTAMIN 1; SPINAL-CORD; INTRACELLULAR CALCIUM; QUANTITATIVE-ANALYSIS; CHOLINERGIC SYSTEM; SKIN INFLAMMATION; FUNCTIONAL-ROLE; CA2+ ENTRY; psoriasis; calcium; ion channels; epidermal cell; immune cell; sensory neuron
- ISSN
- 1661-6596
- URI
- https://pubs.kist.re.kr/handle/201004/149497
- DOI
- 10.3390/ijms25052756
- Appears in Collections:
- KIST Article > 2024
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