TABLE 1.
Clinical and biological features of retinal diseases and confirmed galectin involvement. See main text for additional information.
| Diseases of the retina | Clinical features | Biological features | Galectins involved | |
|---|---|---|---|---|
| Physical damage | Retinal tear | Floaters; Photopsia; Vitreous Haemorrhage; Can result in retinal detachment Landau and Kurz-Levin (2011) | Vitreous liquifies with age and eventually detaches from the retina Landau and Kurz-Levi (2011) | — |
| Retinal detachment | Light flashes, Floaters; Photopsia; Blurred vision; Reduced peripheral vision Landau and Kurz-Levin, (2011) | Rhegmatogenous (most common): Caused by hole in the retina. | Gal-3 accumulation in subretinal fluid of patients with rhegmatogenous retinal detachment Poulsen et al. (2020) | |
| Tractional (e.g. poorly controlled diabetes): Caused by traction from scar tissue on the retinal surface | ||||
| Exudative: Not caused by holes or tears, but often by tumours or inflammation Landau and Kurz-Levin (2011); Steelman and Li (2014) | ||||
| Macular hole | Blurring; Distortion | Full-thickness defect of retina involving fovea Ittarat et al. (2020) | — | |
| Proliferative Vitreoretinopathy (PVR) | Blinding complication of fibrovascular proliferation | Proliferative and inflammatory response of a variety of retinal cells–RPE undergo EMT Alge et al. (2006); Priglinger et al. (2016) | Gal-1 and Gal-3 reduce RPE cell adhesion and spreading Alge et al. (2006); Priglinger et al. (2016) | |
| Epiretinal membrane | Metamorphopsias and central vision impairment | Abnormal growth of tissues on the retinal surface Wang et al. (2016) | No direct evidence for galectin, but key role of Gal-3 in fibrosis Slack et al., (2021) | |
| Complex, multifactorial | Diabetic Retinopathy (DR) | Microaneurysms; Intraretinal haemorrhages; Cotton-wool spots; Venous beading; Vascular loops | Degeneration and loss of pericytes; Proliferation of endothelial cells and thickening of the basement membrane; Capillary occlusion and reduced capillary flow; Inflammation; Increased platelet stickiness and aggregation; Increased production of angiogenic factors, especially VEGF Antonetti et al., (2021). | Gal-1 upregulated in the vitreous and aqueous humour of PDR patients Abu El-Asrar and Ahmed, (2020);Kanda et al., (2017); Ridano et al., (2017) |
| Gal-1 is upregulated in retinal tissue of mice with features of DR Kanda et al., (2017) | ||||
| Gal-1 upregulated in neovascular tufts of OIR mice Liu et al., (2009) | ||||
| Gal-3 KO mice showed less retinal disease Canning et al. (2007) | ||||
| Retinal vein occlusion (RVO) | Blocked central or branch retinal vein causing widespread retinal haemorrhages and macular oedema (Blair and Czyz (2020)) | Neovascular complications | Vascular complications similar to DR/DMO, indicating Gal-1 involvement (see main text) | |
| Gal-3 may protect retina as it does in ischemic stroke Wesley et al. (2020) | ||||
| Retinopathy of prematurity (ROP) | Late stages may present with leucocoria (white reflex); Nystagmus with abnormal eye movements; Bilateral retinal detachment; Falciform fold and pthisis bulbi Dogra et al. (2017) | Delayed retinal vascular development due to hyperoxia and low serum IGF1 in premature babies; Reflex vasoconstriction; Pathologic angiogenesis; High VEGF in the vitreous Margalit and Srinivas (2003) | Galectins not directly involved, but ROP management uses anti-VEGFs, suggesting roles for galectins (see main text) | |
| Hypertensive Retinopathy (HR) | Mild or vasoconstrictive (silver or copper wiring) | Mild–retinal arterial narrowing of the vessels or sclerosis; moderate–additional intimal thickening and arterial narrowing; focal or diffuse arterial wall opacification Malignant–optic nerve swelling Harjasouliha et al. (2017); Kabedi et al. (2014); Tsukikawa and Stacey (2020) | — | |
| Moderate or sclerotic phase (hemorrhages, microaneurysms, cotton-wool spots, exudates) | ||||
| Malignant or exudative phase (moderate retinopathy and optic disk swelling) | ||||
| Age-related macular degeneration (AMD) | Dry (non-neovascular)–slow but progressive decrease in visual acuity, increasing light sensitivity, and reading difficulties | Dry–yellow lesions (drusen) below the RPE, atrophy or hyperpigmentation of the RPE | Gal-1 upregulated in a model of wet AMD Wu et al. (2019) | |
| Wet (neovascular)–sudden, often quite marked, decrease in visual acuity; can results in permanent reduction of vision as well as a central scotoma | Wet–neovascular growth of the choroid; bleeding and exudation from these vessels can damage the outer retina, leading to photoreceptor degeneration Margalit and Srinivas (2003); Landau and Kurz-Levin (2011) | Gal-2, -7, -8 upregulated in RPE/choroid samples of some forms AMD; Gal-8, -12 downregulated in neuroretina of pre-AMD patients, and Gal-3 upregulated in most forms of AMD Newman et al. (2012) | ||
| Gal-3 upregulated in choroid samples from advanced dry AMD Yuan et al. (2010) | ||||
| Inherited retinal diseases | Retinitis Pigmentosa (RP) | Signs include optic nerve pallor, constricted retinal vessels, and bone spicule pigmentation in the periphery | Progressive loss of retinal rod photoreceptor cells followed by subsequent degeneration of cones→ increased reduction of retinal function and eventually retinal atrophy Hartong et al. (2006);Landau and Kurz-Levin (2011); Margalit and Srinivas (2003). | Gal-3 expression elevated in Müller cells in mouse model of RP Roesch et al. (2012) |