Ion channels in dry eye disease.
Dry eye disease
electrolytes
ion channels
ions
transient receptor potential
Journal
Indian journal of ophthalmology
ISSN: 1998-3689
Titre abrégé: Indian J Ophthalmol
Pays: India
ID NLM: 0405376
Informations de publication
Date de publication:
04 2023
04 2023
Historique:
medline:
10
4
2023
entrez:
7
4
2023
pubmed:
8
4
2023
Statut:
ppublish
Résumé
Dry eye disease (DED) which affects millions of people worldwide is an ocular surface disease that is strongly associated with pain, discomfort, and visual disturbances. Altered tear film dynamics, hyperosmolarity, ocular surface inflammation, and neurosensory abnormalities are the key contributors to DED pathogenesis. The presence of discordance between signs and symptoms of DED in patients and refractoriness to current therapies in some patients underpin the need for studying additional contributors that can be modulated. The presence of electrolytes or ions including sodium, potassium, chloride, bicarbonate, calcium, and magnesium in the tear fluid and ocular surface cells contribute to ocular surface homeostasis. Ionic or electrolyte imbalance and osmotic imbalance have been observed in DED and feed-forward interaction between ionic imbalances and inflammation alter cellular processes in the ocular surface resulting in DED. Ionic balances in various cellular and intercellular compartments are maintained by dynamic transport via ion channel proteins present in cell membranes. Hence, alterations in the expression and/or activity of about 33 types of ion channels that belong to voltage-gated channels, ligand-gated channels, mechanosensitive ion channel, aquaporins, chloride ion channel, sodium-potassium-chloride pumps or cotransporters have been investigated in the context of ocular surface health and DED in animal and/or human subjects. An increase in the expression or activity of TRPA1, TRPV1, Nav1.8, KCNJ6, ASIC1, ASIC3, P2X, P2Y, and NMDA receptor have been implicated in DED pathogenesis, whereas an increase in the expression or activity of TRPM8, GABA
Identifiants
pubmed: 37026252
pii: IndianJOphthalmol_2023_71_4_1215_373518
doi: 10.4103/IJO.IJO_3020_22
pmc: PMC10276728
doi:
Substances chimiques
Chlorides
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1215-1226Déclaration de conflit d'intérêts
None
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