Acrolein: A Potential Mediator of Oxidative Damage in Diabetic Retinopathy
Diabetic retinopathy (DR) is the leading cause of vision loss among working-age adults. Extensive evidences have documented that oxidative stress mediates a critical role in the pathogenesis of DR. Acrolein, a product of polyamines oxidation and lipid peroxidation, has been demonstrated to be involv...
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description | Diabetic retinopathy (DR) is the leading cause of vision loss among working-age adults. Extensive evidences have documented that oxidative stress mediates a critical role in the pathogenesis of DR. Acrolein, a product of polyamines oxidation and lipid peroxidation, has been demonstrated to be involved in the pathogenesis of various human diseases. Acrolein's harmful effects are mediated through multiple mechanisms, including DNA damage, inflammation, ROS formation, protein adduction, membrane disruption, endoplasmic reticulum stress, and mitochondrial dysfunction. Recent investigations have reported the involvement of acrolein in the pathogenesis of DR. These studies have shown a detrimental effect of acrolein on the retinal neurovascular unit under diabetic conditions. The current review summarizes the existing literature on the sources of acrolein, the impact of acrolein in the generation of oxidative damage in the diabetic retina, and the mechanisms of acrolein action in the pathogenesis of DR. The possible therapeutic interventions such as the use of polyamine oxidase inhibitors, agents with antioxidant properties, and acrolein scavengers to reduce acrolein toxicity are also discussed. |
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Priya</creator><creatorcontrib>Alfarhan, Moaddey ; Jafari, Eissa ; Narayanan, S. Priya</creatorcontrib><description>Diabetic retinopathy (DR) is the leading cause of vision loss among working-age adults. Extensive evidences have documented that oxidative stress mediates a critical role in the pathogenesis of DR. Acrolein, a product of polyamines oxidation and lipid peroxidation, has been demonstrated to be involved in the pathogenesis of various human diseases. Acrolein's harmful effects are mediated through multiple mechanisms, including DNA damage, inflammation, ROS formation, protein adduction, membrane disruption, endoplasmic reticulum stress, and mitochondrial dysfunction. Recent investigations have reported the involvement of acrolein in the pathogenesis of DR. These studies have shown a detrimental effect of acrolein on the retinal neurovascular unit under diabetic conditions. The current review summarizes the existing literature on the sources of acrolein, the impact of acrolein in the generation of oxidative damage in the diabetic retina, and the mechanisms of acrolein action in the pathogenesis of DR. The possible therapeutic interventions such as the use of polyamine oxidase inhibitors, agents with antioxidant properties, and acrolein scavengers to reduce acrolein toxicity are also discussed.</description><identifier>ISSN: 2218-273X</identifier><identifier>EISSN: 2218-273X</identifier><identifier>DOI: 10.3390/biom10111579</identifier><identifier>PMID: 33233661</identifier><language>eng</language><publisher>BASEL: Mdpi</publisher><subject>Acrolein ; Antioxidants ; Biochemistry & Molecular Biology ; Cholesterol ; Chromatography ; Diabetes ; Diabetes mellitus ; Diabetic retinopathy ; Disease ; DNA damage ; Endoplasmic reticulum ; Fatty acids ; Hemoglobin ; Hyperglycemia ; Life Sciences & Biomedicine ; Lipid peroxidation ; Lipids ; Membrane proteins ; Metabolism ; Metabolites ; Mitochondria ; Neurodegeneration ; Oxidation ; Oxidative stress ; Pathogenesis ; Physiological aspects ; Polyamine oxidase ; polyamine oxidation ; Polyamines ; Retina ; Retinopathy ; Review ; Science & Technology ; Therapeutic applications ; Toxicity ; Triglycerides ; Urine ; vision</subject><ispartof>Biomolecules (Basel, Switzerland), 2020-11, Vol.10 (11), p.1579, Article 1579</ispartof><rights>COPYRIGHT 2020 MDPI AG</rights><rights>2020. 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Priya</creatorcontrib><title>Acrolein: A Potential Mediator of Oxidative Damage in Diabetic Retinopathy</title><title>Biomolecules (Basel, Switzerland)</title><addtitle>BIOMOLECULES</addtitle><addtitle>Biomolecules</addtitle><description>Diabetic retinopathy (DR) is the leading cause of vision loss among working-age adults. Extensive evidences have documented that oxidative stress mediates a critical role in the pathogenesis of DR. Acrolein, a product of polyamines oxidation and lipid peroxidation, has been demonstrated to be involved in the pathogenesis of various human diseases. Acrolein's harmful effects are mediated through multiple mechanisms, including DNA damage, inflammation, ROS formation, protein adduction, membrane disruption, endoplasmic reticulum stress, and mitochondrial dysfunction. Recent investigations have reported the involvement of acrolein in the pathogenesis of DR. These studies have shown a detrimental effect of acrolein on the retinal neurovascular unit under diabetic conditions. The current review summarizes the existing literature on the sources of acrolein, the impact of acrolein in the generation of oxidative damage in the diabetic retina, and the mechanisms of acrolein action in the pathogenesis of DR. The possible therapeutic interventions such as the use of polyamine oxidase inhibitors, agents with antioxidant properties, and acrolein scavengers to reduce acrolein toxicity are also discussed.</description><subject>Acrolein</subject><subject>Antioxidants</subject><subject>Biochemistry & Molecular Biology</subject><subject>Cholesterol</subject><subject>Chromatography</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetic retinopathy</subject><subject>Disease</subject><subject>DNA damage</subject><subject>Endoplasmic reticulum</subject><subject>Fatty acids</subject><subject>Hemoglobin</subject><subject>Hyperglycemia</subject><subject>Life Sciences & Biomedicine</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Membrane proteins</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Mitochondria</subject><subject>Neurodegeneration</subject><subject>Oxidation</subject><subject>Oxidative stress</subject><subject>Pathogenesis</subject><subject>Physiological aspects</subject><subject>Polyamine oxidase</subject><subject>polyamine oxidation</subject><subject>Polyamines</subject><subject>Retina</subject><subject>Retinopathy</subject><subject>Review</subject><subject>Science & Technology</subject><subject>Therapeutic applications</subject><subject>Toxicity</subject><subject>Triglycerides</subject><subject>Urine</subject><subject>vision</subject><issn>2218-273X</issn><issn>2218-273X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AOWDO</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNks9rFDEUxwdRbKm9eZYBL4Ku5sdMZuKhsGyrVioVUfAWXjIv2ywzyZrJ1Pa_N9uty9aTISQh-bxv3ku-RfGckrecS_JOuzBQQimtG_moOGSMtjPW8J-P99YHxfE4rkhube6MPy0OOGecC0EPi89zE0OPzr8v5-XXkNAnB335BTsHKcQy2PLyxnWQ3DWWpzDAEkvny1MHGpMz5bc8-rCGdHX7rHhioR_x-H4-Kn58OPu--DS7uPx4vphfzExNRJoxjZpLBtJK0VUMAUUrLOl4ZQivUVNEYAQ0q0hD2qqTQljd5IgKGZea8qPifKvbBVipdXQDxFsVwKm7jRCXCmLOrUdl0dS1pvUmtEKwYLGRqFnXtsQaTbLWyVZrPekBO5PLj9A_EH144t2VWoZr1QgpGyqywKt7gRh-TTgmNbjRYN-DxzCNilWiojL_lczoy3_QVZiiz091RzFKWL1HLSEX4LwN-V6zEVVzUQnKayaqTL3ZUvn3xjGi3aVMido4Q-07I-Mv9svcwX99kIF2C_xGHexoHHqDOyxbp5asYe3GRIQuXMp-CH4RJp9y6Ov_D-V_AOB302A</recordid><startdate>20201120</startdate><enddate>20201120</enddate><creator>Alfarhan, Moaddey</creator><creator>Jafari, Eissa</creator><creator>Narayanan, S. 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Priya</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acrolein: A Potential Mediator of Oxidative Damage in Diabetic Retinopathy</atitle><jtitle>Biomolecules (Basel, Switzerland)</jtitle><stitle>BIOMOLECULES</stitle><addtitle>Biomolecules</addtitle><date>2020-11-20</date><risdate>2020</risdate><volume>10</volume><issue>11</issue><spage>1579</spage><pages>1579-</pages><artnum>1579</artnum><issn>2218-273X</issn><eissn>2218-273X</eissn><abstract>Diabetic retinopathy (DR) is the leading cause of vision loss among working-age adults. Extensive evidences have documented that oxidative stress mediates a critical role in the pathogenesis of DR. Acrolein, a product of polyamines oxidation and lipid peroxidation, has been demonstrated to be involved in the pathogenesis of various human diseases. Acrolein's harmful effects are mediated through multiple mechanisms, including DNA damage, inflammation, ROS formation, protein adduction, membrane disruption, endoplasmic reticulum stress, and mitochondrial dysfunction. Recent investigations have reported the involvement of acrolein in the pathogenesis of DR. These studies have shown a detrimental effect of acrolein on the retinal neurovascular unit under diabetic conditions. The current review summarizes the existing literature on the sources of acrolein, the impact of acrolein in the generation of oxidative damage in the diabetic retina, and the mechanisms of acrolein action in the pathogenesis of DR. The possible therapeutic interventions such as the use of polyamine oxidase inhibitors, agents with antioxidant properties, and acrolein scavengers to reduce acrolein toxicity are also discussed.</abstract><cop>BASEL</cop><pub>Mdpi</pub><pmid>33233661</pmid><doi>10.3390/biom10111579</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acrolein Antioxidants Biochemistry & Molecular Biology Cholesterol Chromatography Diabetes Diabetes mellitus Diabetic retinopathy Disease DNA damage Endoplasmic reticulum Fatty acids Hemoglobin Hyperglycemia Life Sciences & Biomedicine Lipid peroxidation Lipids Membrane proteins Metabolism Metabolites Mitochondria Neurodegeneration Oxidation Oxidative stress Pathogenesis Physiological aspects Polyamine oxidase polyamine oxidation Polyamines Retina Retinopathy Review Science & Technology Therapeutic applications Toxicity Triglycerides Urine vision |
title | Acrolein: A Potential Mediator of Oxidative Damage in Diabetic Retinopathy |
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