Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Treatment with isotretinoin inhibits lipofuscin accumulation in a mouse model of recessive Stargardt's macular degeneration

1 Apr 2003

Abstract excerpt

Recessive Stargardt's macular degeneration is an inherited blinding disease of children caused by mutations in the ABCR gene. The primary pathologic defect in Stargardt's disease is accumulation of toxic lipofuscin pigments such as N-retinylidene-N-retinylethanolamine (A2E) in cells of the retinal pigment epithelium. This accumulation appears to be responsible for the photoreceptor death and severe visual loss in...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Retinal Development and Disorders
Share to Retinal Diseases and Treatments
Share to Retinoids in leukemia and cellular processes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 12671074
DOI: 10.1073/pnas.0737855100

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Treatment with isotretinoin inhibits lipofuscin accumulation in a mouse model of recessive Stargardt's macular degenerationPMID 12671074Read ↗

Light exposure stimulates formation of A2E oxiranes in a mouse model of Stargardt's macular degenerationSemantic proximity Read ↗

Delayed dark-adaptation and lipofuscin accumulation in abcr+/- mice: implications for involvement of ABCR in age-related macular degeneration.Semantic proximity Read ↗

C20-D3-vitamin A Slows Lipofuscin Accumulation and Electrophysiological Retinal Degeneration in a Mouse Model of Stargardt DiseaseSemantic proximity Read ↗

Correction of the disease phenotype in the mouse model of Stargardt disease by lentiviral gene therapy.Semantic proximity Read ↗

Accelerated Accumulation of Lipofuscin Pigments in the RPE of a Mouse Model for<i>ABCA4</i>-Mediated Retinal Dystrophies following Vitamin A SupplementationSemantic proximity Read ↗

Retinal cone and rod photoreceptor cells exhibit differential susceptibility to light‐induced damageSemantic proximity Read ↗

Complement System Dysregulation and Inflammation in the Retinal Pigment Epithelium of a Mouse Model for Stargardt Macular DegenerationSemantic proximity Read ↗

All-trans retinal levels and formation of lipofuscin precursors after bleaching in rod photoreceptors from wild type and Abca4-/- mice.Semantic proximity Read ↗

Rescue of the Stargardt Disease phenotype in <i>Abca4</i> knockout mice through dietary modulation of the vitamin A receptor RBPR2Semantic proximity Read ↗

Light damage in Abca4 and Rpe65rd12 mice.Semantic proximity Read ↗

Fundus Autofluorescence in the<i>Abca4<sup>−/−</sup></i>Mouse Model of Stargardt Disease—Correlation With Accumulation of A2E, Retinal Function, and HistologySemantic proximity Read ↗

ABCR, the ATP-binding Cassette Transporter Responsible for Stargardt Macular Dystrophy, Is an Efficient Target of All-trans-retinal-mediated Photooxidative Damage in VitroSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.