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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004008naa a2200637 4500
001oai:lup.lub.lu.se:f2ab4d45-ad23-41e4-a819-ad50a4bb4636
003SwePub
008160401s2008 | |||||||||||000 ||eng|
0247 a https://lup.lub.lu.se/record/14157652 URI
0247 a https://doi.org/10.1007/s12035-008-8045-92 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a for2 swepub-publicationtype
072 7a ref2 swepub-contenttype
1001 a Sancho-Pelluz, J.4 aut
2451 0a Photoreceptor Cell Death Mechanisms in Inherited Retinal Degeneration
264 c 2008-11-04
264 1b Springer Science and Business Media LLC,c 2008
520 a Photoreceptor cell death is the major hallmark of a group of human inherited retinal degenerations commonly referred to as retinitis pigmentosa (RP). Although the causative genetic mutations are often known, the mechanisms leading to photoreceptor degeneration remain poorly defined. Previous research work has focused on apoptosis, but recent evidence suggests that photoreceptor cell death may result primarily from non-apoptotic mechanisms independently of AP1 or p53 transcription factor activity, Bcl proteins, caspases, or cytochrome c release. This review briefly describes some animal models used for studies of retinal degeneration, with particular focus on the rd1 mouse. After outlining the major features of different cell death mechanisms in general, we then compare them with results obtained in retinal degeneration models, where photoreceptor cell death appears to be governed by, among other things, changes in cyclic nucleotide metabolism, downregulation of the transcription factor CREB, and excessive activation of calpain and PARP. Based on recent experimental evidence, we propose a putative non-apoptotic molecular pathway for photoreceptor cell death in the rd1 retina. The notion that inherited photoreceptor cell death is driven by non-apoptotic mechanisms may provide new ideas for future treatment of RP.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
653 a Retina
653 a rd1
653 a PARP
653 a CREB
653 a Oxidative stress
653 a Calpain
653 a cGMP
653 a AIF
653 a Calcium
653 a rd2
653 a rds
653 a APOPTOSIS-INDUCING FACTOR
653 a ROD CGMP-PHOSPHODIESTERASE
653 a ENDOPLASMIC-RETICULUM STRESS
653 a ELEMENT-BINDING PROTEIN
653 a CAMP EARLY
653 a REPRESSOR
653 a RD1 MOUSE RETINA
653 a MEDIATED PROGRAMMED NECROSIS
653 a CALCIUM-CHANNEL BLOCKER
653 a NITRIC-OXIDE SYNTHASE
653 a D-CIS-DILTIAZEM
7001 a Arango-Gonzalez, B.4 aut
7001 a Kustermann, S.4 aut
7001 a Romero, F. J.4 aut
7001 a van Veen, Theou Lund University,Lunds universitet,Oftalmologi, Lund,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Ophthalmology, Lund,Section IV,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)oft-tve
7001 a Zrenner, E.4 aut
7001 a Ekström, Peru Lund University,Lunds universitet,Oftalmologi, Lund,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Ophthalmology, Lund,Section IV,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)zoof-pek
7001 a Paquet-Durand, F.4 aut
7102 a Oftalmologi, Lundb Sektion IV4 org
7730 t Molecular Neurobiologyd : Springer Science and Business Media LLCg 38:3, s. 253-269q 38:3<253-269x 1559-1182x 0893-7648
8564 u http://dx.doi.org/10.1007/s12035-008-8045-9y FULLTEXT
8564 8u https://lup.lub.lu.se/record/1415765
8564 8u https://doi.org/10.1007/s12035-008-8045-9

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