Spare the rod and spoil the eye

Arden, G B; Sidman, Richard L.; Arap, Wadih; Schlingemann, Reinier O.

doi:10.1136/bjo.2004.062547

Cited by 141 publications

(119 citation statements)

References 80 publications

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“…In addition, a number of inflammatory and immunomodulatory processes, chronic oxidative insult, proteolysis, and cytoskeleton remodeling, have been implicated in its formation (Joshi, Agrawal, & Christoforidis, 2013; Pollreisz et al, 2013). Metabolically, the retina is the most oxygen‐consuming tissue in the human body (Arden, Sidman, Arap, & Schlingemann, 2005). Therefore, metabolic stress and an altered microvascular retinal blood flow, together with genetic and lifestyle‐related factors, such as smoking, could also play a role in iERM formation (Salminen et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Systems pathology analysis identifies neurodegenerative nature of age‐related vitreoretinal interface diseases

et al. 2018

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Aging is a phenomenon that is associated with profound medical implications. Idiopathic epiretinal membrane (iEMR) and macular hole (MH) are the major vision‐threatening vitreoretinal diseases affecting millions of aging people globally, making these conditions an important public health issue. iERM is characterized by fibrous tissue developing on the surface of the macula, which leads to biomechanical and biochemical macular damage. MH is a small breakage in the macula and is associated with many ocular conditions. Although several individual factors and pathways are suggested, a systems pathology level understanding of the molecular mechanisms underlying these disorders is lacking. Therefore, we performed mass spectrometry‐based label‐free quantitative proteomics analysis of the vitreous proteomes from patients with iERM and MH to identify the key proteins, as well as the multiple interconnected biochemical pathways, contributing to the development of these diseases. We identified a total of 1,014 unique proteins, many of which are linked to inflammation and the complement cascade, revealing the inflammation processes in retinal diseases. Additionally, we detected a profound difference in the proteomes of iEMR and MH compared to those of diabetic retinopathy with macular edema and rhegmatogenous retinal detachment. A large number of neuronal proteins were present at higher levels in the iERM and MH vitreous, including neuronal adhesion molecules, nervous system development proteins, and signaling molecules, pointing toward the important role of neurodegenerative component in the pathogenesis of age‐related vitreoretinal diseases. Despite them having marked similarities, several unique vitreous proteins were identified in both iERM and MH, from which candidate targets for new diagnostic and therapeutic approaches can be provided.

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Section: Introductionmentioning

confidence: 99%

Systems pathology analysis identifies neurodegenerative nature of age‐related vitreoretinal interface diseases

et al. 2018

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“…34,35 The trans-lid illumination caused by the masks would therefore produce minimal changes in melatonin. The only known way for such weak light to reverse retinal changes is thus via the hypothesis already advanced, 21 that during dark adaptation, rod metabolic activity increases and the resulting hypoxia stimulates the production of cytokines that cause retinal damage. Thus the study may be considered a proof of principle.…”

Section: Implications For the Pathophysiology Of Drmentioning

confidence: 99%

“…There is Fast Track Paper Fast Track Paper considerable evidence to support this view. [13][14][15][16][17][18] These and other observations have led to a different proposal about the pathophysiology of DR. 19,[20][21][22] The oxygen demand of rods, in the outer retina, is much increased in darkness 6,7,13,[23][24][25] and this in turn causes a reduction in inner retinal oxygen tension. 11,25 It has been suggested that the increasing inner retinal hypoxia in diabetes causes the upregulation of cytokines, most importantly VEGF, to a degree that produces damage to small retinal vessels, thus reducing local capillary blood flow and increasing hypoxia in a vicious circle.…”

Section: Introductionmentioning

confidence: 99%

Regression of early diabetic macular oedema is associated with prevention of dark adaptation

Arden

Jyothi

Hogg

et al. 2011

Eye

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Hypothesis Dark-adapted rods consume oxygen at high rates and light adaptation decreases this oxygen burden and can have therapeutic effects on diabetic macular oedema (DMO). Methods Patients with mild nonproliferative diabetic retinopathy (DR) and early, untreated non-sight-threatening DMO slept for 6 months wearing masks that illuminated the eyelid of one closed eye by 505 nm light. Exclusion criteria were any concomitant eye disease, DR 4ETDRS grade 35, and other systemic diseases. Primary outcome: change of OCT retinal thickness in the local region where oedema was present. Results A total of 34 out of 40 patients completed the study. Mean baseline OCT macular cube thickness was equivalent for study and fellow eyes. But study eyes had a greater mean thickness in the central subfield zone 1 (282±53 lm) vs (256±19 lm) the fellow eyes. Twenty-eight study eyes showed intraretinal cysts compared with nine in the fellow eyes. At 6 months, only 19 study eyes had cysts while cysts were seen in 20 fellow eyes. After 6 months, the worst affected ETDRS zone and the central subfield zone 1 reduced in thickness in study eyes only by 12 lm (95% CI 20 to À7, P ¼ 0.01). The secondary outcomes of change in visual acuity, achromatic contrast sensitivity, and microperimetric thresholds improved significantly in study eyes and deteriorated in fellow eyes. Conclusions Sleeping in dim light that can keep rods light adapted may reverse the changes of DMO.

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“…10 The vascular supply to the outer part of the retina is through the choroid and that to the inner part is from the retinal vessels. Choroidal vessels are among the tissues with the fastest blood flow and are innervated by a large number of sympathetic nerves, 11 but they lack autonomic innervation; in contrast, retinal vessels have slow blood flow and large oxygen intake, and therefore the inner part of the retina is sensitive to hypoxia.…”

Section: Introductionmentioning

confidence: 99%

Retinal and choroidal thickness evaluation by SD-OCT in adults with obstructive sleep apnea-hypopnea syndrome (OSAS)

Chen

Wang

Zhang

et al. 2014

Eye

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Objective To assess the macular retina and choroidal thickness change in patients with obstructive sleep apnea-hypopnea syndrome (OSAS) with no significant symptoms and pathological changes in the fundus using spectral domain-optical coherence tomography. Methods This prospective, observational case-control study consisted of 53 eyes of 53 patients with OSAS and 12 eyes of 12 age-matched controls. Macular and choroidal thicknesses were measured by optical coherence tomography. Results The foveal and nasal macular thicknesses were significantly different between four groups (P ¼ 0.001, P ¼ 0.016). The foveal thickness of the control group was significantly thinner than that of the severe group (P ¼ 0.000). The nasal macular thickness of the control group was significantly thinner than that of the severe group (P ¼ 0.008). A significant correlation was found between oxygen desaturation index (ODI) and macular center thickness (r ¼ 0.357, R 2 ¼ 0.127, P ¼ 0.004), with an ODI coefficient of 0.457 (P ¼ 0.004). Similarly, a significant correlation was found between ODI and nasal macular thickness (r ¼ 0.265, R 2 ¼ 0.070, P ¼ 0.033), with an ODI coefficient of 0.233 (P ¼ 0.033). The subfoveal choroidal thickness was significantly different among the groups (F ¼ 3.657, P ¼ 0.017). The subfoveal choroidal thickness of the severe group was significantly thinner than that of the control group, mild group, and moderate group (P ¼ 0.023, 0.006, and 0.036, respectively). The choroidal thickness 1 mm nasal to the fovea was significantly different between the groups after correcting for age and diopter (F ¼ 3.411, P ¼ 0.023). The choroidal thickness 1 mm nasal to the fovea was significantly thinner in the severe group compared with the control group and mild group (P ¼ 0.013 and 0.010, respectively). Choroidal thickness was significantly correlated with diopter (r ¼ 0.520, R 2 ¼ 0.270, Po0.001), with a coefficient of 0.327 (Po0.001), and with ODI (r ¼ 0.520, R 2 ¼ 0.165, P ¼ 0.001), with a coefficient of À 0.370 (P ¼ 0.001). Conclusions OSAS patients showed decreased foveal and nasal macular thickness, similar to the subfoveal and nasal choroidal thickness. These findings suggest that, because of intermittent hypoxia, OSAS might change the retinal and choroidal blood supply.

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Spare the rod and spoil the eye

Cited by 141 publications

References 80 publications

Systems pathology analysis identifies neurodegenerative nature of age‐related vitreoretinal interface diseases

Systems pathology analysis identifies neurodegenerative nature of age‐related vitreoretinal interface diseases

Regression of early diabetic macular oedema is associated with prevention of dark adaptation

Retinal and choroidal thickness evaluation by SD-OCT in adults with obstructive sleep apnea-hypopnea syndrome (OSAS)

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