The role of UV irradiation in the progression of diabetic retinopathy

Liat Avdian, Alon Harris, R. Shane Tubbs, Marios Loukas, Ghaffar Shokouhi, Kamyar Ghabili, Paul S. Agutter, Brent Siesky, Yochai Shoshani, Mohammadali M. Shoja

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Diabetic retinopathy is a major cause of blindness. Underlying pathogenicmechanisms that have been suggested include the non-enzymatic glycosylation pathwayand production of advanced glycation end-products (AGEs), retinal neurodegeneration and inflammation, and enhanced reactive oxygen species (ROS) generation. Here, theauthors discuss how the UV component of solar radiation may potentially enhance theprogression of diabetic retinopathy. The mechanisms we suggest are: (1) In hightemperatureenvironments with intense solar radiation, the amount of UV reaching theretina is sufficient to increase de novo ROS generation. (2) Under UV-A irradiation,AGEs generate ROS. (3) Enhanced oxidative stress promotes generation of AGEs. (4)UV-B may enhance intraocular inflammation (production of endothelin and IL-6)in DR patients, and this in turn may accelerate AGE generation. (5) UV-B and ROSindependently up-regulate VEGF expression, inducing fibrovascular proliferation andinflammation. (6) ROS induce apoptosis of the retinal neurons and pericytes. (7)Oxidation of the glycated proteins and lipids produces potentially toxic substanceswithin the retina. Thus, UV irradiation could enhance the progression of diabeticretinopathy, so strategies to limit UV exposure such as wearing protective sunglasses orusing photochromic lenses that could attenuate this progression will become increasinglyimportant as humans are exposed to greater levels of solar radiation.

Original languageEnglish
Title of host publicationHypotheses in Clinical Medicine
PublisherNova Science Publishers, Inc.
Pages438-444
Number of pages7
ISBN (Print)9781622572762
StatePublished - 2013

Fingerprint

Advanced Glycosylation End Products
Diabetic Retinopathy
Reactive Oxygen Species
Radiation
Inflammation
Retinal Neurons
Pericytes
Poisons
Endothelins
Blindness
Glycosylation
Vascular Endothelial Growth Factor A
Lenses
Retina
Interleukin-6
Oxidative Stress
Up-Regulation
Apoptosis
Lipids
Proteins

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Avdian, L., Harris, A., Tubbs, R. S., Loukas, M., Shokouhi, G., Ghabili, K., ... Shoja, M. M. (2013). The role of UV irradiation in the progression of diabetic retinopathy. In Hypotheses in Clinical Medicine (pp. 438-444). Nova Science Publishers, Inc..

The role of UV irradiation in the progression of diabetic retinopathy. / Avdian, Liat; Harris, Alon; Tubbs, R. Shane; Loukas, Marios; Shokouhi, Ghaffar; Ghabili, Kamyar; Agutter, Paul S.; Siesky, Brent; Shoshani, Yochai; Shoja, Mohammadali M.

Hypotheses in Clinical Medicine. Nova Science Publishers, Inc., 2013. p. 438-444.

Research output: Chapter in Book/Report/Conference proceedingChapter

Avdian, L, Harris, A, Tubbs, RS, Loukas, M, Shokouhi, G, Ghabili, K, Agutter, PS, Siesky, B, Shoshani, Y & Shoja, MM 2013, The role of UV irradiation in the progression of diabetic retinopathy. in Hypotheses in Clinical Medicine. Nova Science Publishers, Inc., pp. 438-444.
Avdian L, Harris A, Tubbs RS, Loukas M, Shokouhi G, Ghabili K et al. The role of UV irradiation in the progression of diabetic retinopathy. In Hypotheses in Clinical Medicine. Nova Science Publishers, Inc. 2013. p. 438-444
Avdian, Liat ; Harris, Alon ; Tubbs, R. Shane ; Loukas, Marios ; Shokouhi, Ghaffar ; Ghabili, Kamyar ; Agutter, Paul S. ; Siesky, Brent ; Shoshani, Yochai ; Shoja, Mohammadali M. / The role of UV irradiation in the progression of diabetic retinopathy. Hypotheses in Clinical Medicine. Nova Science Publishers, Inc., 2013. pp. 438-444
@inbook{14bd7e0052424b8480fadd271b5bc1c5,
title = "The role of UV irradiation in the progression of diabetic retinopathy",
abstract = "Diabetic retinopathy is a major cause of blindness. Underlying pathogenicmechanisms that have been suggested include the non-enzymatic glycosylation pathwayand production of advanced glycation end-products (AGEs), retinal neurodegeneration and inflammation, and enhanced reactive oxygen species (ROS) generation. Here, theauthors discuss how the UV component of solar radiation may potentially enhance theprogression of diabetic retinopathy. The mechanisms we suggest are: (1) In hightemperatureenvironments with intense solar radiation, the amount of UV reaching theretina is sufficient to increase de novo ROS generation. (2) Under UV-A irradiation,AGEs generate ROS. (3) Enhanced oxidative stress promotes generation of AGEs. (4)UV-B may enhance intraocular inflammation (production of endothelin and IL-6)in DR patients, and this in turn may accelerate AGE generation. (5) UV-B and ROSindependently up-regulate VEGF expression, inducing fibrovascular proliferation andinflammation. (6) ROS induce apoptosis of the retinal neurons and pericytes. (7)Oxidation of the glycated proteins and lipids produces potentially toxic substanceswithin the retina. Thus, UV irradiation could enhance the progression of diabeticretinopathy, so strategies to limit UV exposure such as wearing protective sunglasses orusing photochromic lenses that could attenuate this progression will become increasinglyimportant as humans are exposed to greater levels of solar radiation.",
author = "Liat Avdian and Alon Harris and Tubbs, {R. Shane} and Marios Loukas and Ghaffar Shokouhi and Kamyar Ghabili and Agutter, {Paul S.} and Brent Siesky and Yochai Shoshani and Shoja, {Mohammadali M.}",
year = "2013",
language = "English",
isbn = "9781622572762",
pages = "438--444",
booktitle = "Hypotheses in Clinical Medicine",
publisher = "Nova Science Publishers, Inc.",

}

TY - CHAP

T1 - The role of UV irradiation in the progression of diabetic retinopathy

AU - Avdian, Liat

AU - Harris, Alon

AU - Tubbs, R. Shane

AU - Loukas, Marios

AU - Shokouhi, Ghaffar

AU - Ghabili, Kamyar

AU - Agutter, Paul S.

AU - Siesky, Brent

AU - Shoshani, Yochai

AU - Shoja, Mohammadali M.

PY - 2013

Y1 - 2013

N2 - Diabetic retinopathy is a major cause of blindness. Underlying pathogenicmechanisms that have been suggested include the non-enzymatic glycosylation pathwayand production of advanced glycation end-products (AGEs), retinal neurodegeneration and inflammation, and enhanced reactive oxygen species (ROS) generation. Here, theauthors discuss how the UV component of solar radiation may potentially enhance theprogression of diabetic retinopathy. The mechanisms we suggest are: (1) In hightemperatureenvironments with intense solar radiation, the amount of UV reaching theretina is sufficient to increase de novo ROS generation. (2) Under UV-A irradiation,AGEs generate ROS. (3) Enhanced oxidative stress promotes generation of AGEs. (4)UV-B may enhance intraocular inflammation (production of endothelin and IL-6)in DR patients, and this in turn may accelerate AGE generation. (5) UV-B and ROSindependently up-regulate VEGF expression, inducing fibrovascular proliferation andinflammation. (6) ROS induce apoptosis of the retinal neurons and pericytes. (7)Oxidation of the glycated proteins and lipids produces potentially toxic substanceswithin the retina. Thus, UV irradiation could enhance the progression of diabeticretinopathy, so strategies to limit UV exposure such as wearing protective sunglasses orusing photochromic lenses that could attenuate this progression will become increasinglyimportant as humans are exposed to greater levels of solar radiation.

AB - Diabetic retinopathy is a major cause of blindness. Underlying pathogenicmechanisms that have been suggested include the non-enzymatic glycosylation pathwayand production of advanced glycation end-products (AGEs), retinal neurodegeneration and inflammation, and enhanced reactive oxygen species (ROS) generation. Here, theauthors discuss how the UV component of solar radiation may potentially enhance theprogression of diabetic retinopathy. The mechanisms we suggest are: (1) In hightemperatureenvironments with intense solar radiation, the amount of UV reaching theretina is sufficient to increase de novo ROS generation. (2) Under UV-A irradiation,AGEs generate ROS. (3) Enhanced oxidative stress promotes generation of AGEs. (4)UV-B may enhance intraocular inflammation (production of endothelin and IL-6)in DR patients, and this in turn may accelerate AGE generation. (5) UV-B and ROSindependently up-regulate VEGF expression, inducing fibrovascular proliferation andinflammation. (6) ROS induce apoptosis of the retinal neurons and pericytes. (7)Oxidation of the glycated proteins and lipids produces potentially toxic substanceswithin the retina. Thus, UV irradiation could enhance the progression of diabeticretinopathy, so strategies to limit UV exposure such as wearing protective sunglasses orusing photochromic lenses that could attenuate this progression will become increasinglyimportant as humans are exposed to greater levels of solar radiation.

UR - http://www.scopus.com/inward/record.url?scp=84895241736&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84895241736&partnerID=8YFLogxK

M3 - Chapter

SN - 9781622572762

SP - 438

EP - 444

BT - Hypotheses in Clinical Medicine

PB - Nova Science Publishers, Inc.

ER -