Vitamin A incorporation into lipofuscin-like inclusions in the retinal pigment epithelium

Katz, Martin L.; Gao, Chun-Lan

doi:10.1016/0047-6374(95)01633-b

Cited by 29 publications

(21 citation statements)

References 10 publications

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“…Lipofuscin may be responsible for oxidative damage to the RPE that results in impaired metabolism and apoptosis characteristic of late AMD (15). Studies suggest that lipofuscin is a manifestation of the balance between production and elimination of partially metabolized substances, mostly lipid peroxide-containing materials (88,89). Thus, the agerelated accumulation of intracellular lipofuscin is an indicator for impairment of lipid degradation processes (90).…”

Section: Discussionmentioning

confidence: 99%

Retinal pigment epithelium, age-related macular degeneration and neurotrophic keratouveitis

Bianchi

Scarinci

Ripandelli

et al. 2012

International Journal of Molecular Medicine

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Abstract. Age-related macular degeneration (AMD) is the leading cause of impaired vision and blindness in the aging population. The aims of our studies were to identify qualitative and quantitative alterations in mitochondria in human retinal pigment epithelium (RPE) from AMD patients and controls and to test the protective effects of pigment epithelium-derived factor (PEDF), a known neurotrophic and antiangiogenic substance, against neurotrophic keratouveitis. Histopathological alterations were studied by means of morphometry, light and electron microscopy. Unexpectedly, morphometric data showed that the RPE alterations noted in AMD may also develop in normal aging, 10-15 years later than appearing in AMD patients. Reduced tear secretion, corneal ulceration and leukocytic infiltration were found in capsaicin (CAP)-treated rats, but this effect was significantly attenuated by PEDF. These findings suggest that PEDF accelerated the recovery of tear secretion and also prevented neurotrophic keratouveitis and vitreoretinal inflammation. PEDF may have a clinical application in inflammatory and neovascular diseases of the eye.

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Section: Discussionmentioning

confidence: 99%

Retinal pigment epithelium, age-related macular degeneration and neurotrophic keratouveitis

Bianchi

Scarinci

Ripandelli

et al. 2012

International Journal of Molecular Medicine

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“…Nev-ertheless, CatD has been shown to play an essential function in lysosomal processing of ROS. 21,36 Thus, it was expected that similar to other lysosomal enzymes, [32][33][34] compromising CatD activity would induce undigested photoreceptor breakdown product accumulation. Indeed in the mcd/mcd model, POS lysosomal processing was impaired 28 and AMD traits were demonstrated, suggesting that AMD is not necessarily a disease caused by a specific genetic mutation or a specific abnormality but it could be the consequence of a variety of changes associated with photoreceptor breakdown product accumulation.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies by this group and others suggested that compromising lysosomal enzyme function leads to undigested photoreceptor breakdown product accumulation in vitro and in vivo. [32][33][34][35] Although accumulation of inactive forms of CatD has been associated with various diseases, CatD has not been linked to any particular eye disease. Nev-ertheless, CatD has been shown to play an essential function in lysosomal processing of ROS.…”

Section: Discussionmentioning

confidence: 99%

Progressive Age-Related Changes Similar to Age-Related Macular Degeneration in a Transgenic Mouse Model

Rakoczy

Zhang

Robertson

et al. 2002

The American Journal of Pathology

157

115

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“…It was shown in animal models that genetic [207,208] and small-molecule [209,210] inhibition of the lysosomal system in the RPE results in increased accumulation of lipofuscin. Hypothetically, lipofuscin accumulation in the RPE can be reduced by stimulation of the lysosomal degradation.…”

Section: Expert Opinionmentioning

confidence: 99%

New therapeutic targets in atrophic age-related macular degeneration

Petrukhin¹

2007

Expert Opinion on Therapeutic Targets

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Age-related macular degeneration (AMD) is the leading cause of blindness in developed countries. There is no effective treatment for the most prevalent atrophic (dry) form of AMD. Atrophic AMD is triggered by abnormalities in the retinal pigment epithelium (RPE) that lies beneath the photoreceptor cells and normally provides critical metabolic support to these light-sensing cells. Secondary to RPE dysfunction, macular rods and cones degenerate leading to the irreversible loss of vision. Oxidative stress, formation of drusen, accumulation of lipofuscin, local inflammation and reactive gliosis represent the pathologic processes implicated in pathogenesis of atrophic AMD. This review discusses potential target areas for small-molecule and biologic intervention, which may lead to development of new therapeutic treatments for atrophic AMD.

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Vitamin A incorporation into lipofuscin-like inclusions in the retinal pigment epithelium

Cited by 29 publications

References 10 publications

Retinal pigment epithelium, age-related macular degeneration and neurotrophic keratouveitis

Retinal pigment epithelium, age-related macular degeneration and neurotrophic keratouveitis

Progressive Age-Related Changes Similar to Age-Related Macular Degeneration in a Transgenic Mouse Model

New therapeutic targets in atrophic age-related macular degeneration

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