NAION or not NAION? A literature review of pathogenesis and differential diagnosis of anterior ischaemic optic neuropathies

Martin-Gutierrez, M. Pilar; Petzold, Axel; Saihan, Zubin

doi:10.1038/s41433-023-02716-4

Cited by 1 publication

(1 citation statement)

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“…Even small changes in intracellular water content and intra/extracellular volume influence protein function, diffusion of extracellular molecules and cellular performance (Epstein, Jedziniak et al 1978, Pasantes-Morales 2016, Nicholson and Hrabetova 2017 while excessive swelling (edema) caused by ischemia, hyponatremia, traumatic brain/ocular/lung injury leads to energy depletion, loss of barrier function and oncotic, necrotic or apoptotic cell death (Platonova, Koltsova et al 2012). Cytotoxic and vascular edema in the eye have been associated with pathologies such as corneal edema, diabetic retinopathy, Posner-Schlossman syndrome (PSS), age-related macular degeneration and vascular occlusion (Pannicke, Iandiev et al 2006, Orduna Rios, Noguez Imm et al 2019, Yan, Li et al 2022, Martin-Gutierrez, Petzold et al 2024. Healthy cells mitigate swelling-induced injury through "regulatory volume decrease" (RVD)extrusion of Na + , K + , Clions and organic osmolytes that may be accompanied by changes in [Ca 2+ ]i (Hoffmann, Lambert et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Osmosensing in trabecular meshwork cells

Baumann,

Yarishkin,

Lakk

et al. 2024

Preprint

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Aqueous humor drainage from the anterior eye constitutes a key determinant of intraocular pressure (IOP) under homeostatic and pathological conditions. Swelling of the trabecular meshwork (TM) increases its flow resistance but the mechanisms that sense and transduce osmotic gradients remain poorly understood. We used optical molecular analyses, optical imaging and electrophysiology to investigate TM osmotransduction and its role in calcium and chloride homeostasis. Anisosmotic conditions elicited proportional changes in TM cell volume. Swelling, but not shrinking, evoked increases in intracellular calcium concentration [Ca2+]TM. Hypotonicity-evoked calcium signals were sensitive to HC067047, a selective blocker of TRPV4 channels, whereas the agonist GSK1016790A promoted swelling under isotonic conditions. TRPV4 inhibition partially suppressed hypotonicity-induced volume increases and reduced the magnitude of the swelling-induced membrane current, with a substantial fraction of the swelling-evoked current abrogated by Cl-channel antagonists DIDS and niflumic acid. The volume-sensing transcriptome of primary human TM cells showed expression of TRPV4, TRPM4, AQP1, and TMEMC3B genes. Cl-channel expression was dominated by ANO6 transcripts, auxiliary levels of ANO3, ANO7 and ANO10 and modest expression of LTTRC genes that encode volume-activated anion channels. Thus, TRPV4-mediated cation influx works with Cl-efflux to sense and respond to osmotic stress, potentially contributing to pathological swelling, calcium overload and intracellular signaling that could exacerbate functional disturbances in inflammatory disease and glaucoma.

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