FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
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Citation
Križaj, D., Cordeiro, S., Strauß, O. (2023). Retinal TRP channels: Cell-type-specific regulators of retinal homeostasis and multimodal integration.  Prog. Retin. Eye Res. 92(): 101114.
FlyBase ID
FBrf0255488
Publication Type
Review
Abstract
Transient receptor potential (TRP) channels are a widely expressed family of 28 evolutionarily conserved cationic ion channels that operate as primary detectors of chemical and physical stimuli and secondary effectors of metabotropic and ionotropic receptors. In vertebrates, the channels are grouped into six related families: TRPC, TRPV, TRPM, TRPA, TRPML, and TRPP. As sensory transducers, TRP channels are ubiquitously expressed across the body and the CNS, mediating critical functions in mechanosensation, nociception, chemosensing, thermosensing, and phototransduction. This article surveys current knowledge about the expression and function of the TRP family in vertebrate retinas, which, while dedicated to transduction and transmission of visual information, are highly susceptible to non-visual stimuli. Every retinal cell expresses multiple TRP subunits, with recent evidence establishing their critical roles in paradigmatic aspects of vertebrate vision that include TRPM1-dependent transduction of ON bipolar signaling, TRPC6/7-mediated ganglion cell phototransduction, TRP/TRPL phototransduction in Drosophila and TRPV4-dependent osmoregulation, mechanotransduction, and regulation of inner and outer blood-retina barriers. TRP channels tune light-dependent and independent functions of retinal circuits by modulating the intracellular concentration of the 2nd messenger calcium, with emerging evidence implicating specific subunits in the pathogenesis of debilitating diseases such as glaucoma, ocular trauma, diabetic retinopathy, and ischemia. Elucidation of TRP channel involvement in retinal biology will yield rewards in terms of fundamental understanding of vertebrate vision and therapeutic targeting to treat diseases caused by channel dysfunction or over-activation.
PubMed ID
PubMed Central ID
PMC9897210 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Prog. Retin. Eye Res.
    Title
    Progress in retinal and eye research
    ISBN/ISSN
    1350-9462 1873-1635
    Data From Reference
    Genes (8)