6533b7d0fe1ef96bd125ae8f
RESEARCH PRODUCT
Evidence for a dysfunction and disease-promoting role of the circadian clock in the diabetic retina.
Laura OebelUte FrederiksenCarsten StichtSimon SpohnKristina SchäferRainer SpessertPatrick Vancurasubject
Blood GlucoseMalemedicine.medical_specialtyCircadian clockCLOCK ProteinsDiseaseChronobiology DisordersPathogenesisCellular and Molecular Neurosciencechemistry.chemical_compoundMiceDiabetes mellitusInternal medicineCircadian ClocksRNA Ribosomal 18SMedicineAnimalsRNA MessengerRetinaDiabetic Retinopathybusiness.industryGlyceraldehyde-3-Phosphate DehydrogenasesRetinalDiabetic retinopathymedicine.diseaseSensory SystemsPathophysiologyCircadian RhythmMice Inbred C57BLOphthalmologyDisease Models Animalmedicine.anatomical_structureEndocrinologychemistryMicroscopy FluorescenceFemalebusinessdescription
Diabetic retinopathy is a major complication of chronic hyperglycemia and a leading cause of blindness in developed countries. In the present study the interaction between diabetes and retinal clocks was investigated in mice. It was seen that in the db/db mouse - a widely used animal model of diabetic retinopathy - clock function and circadian regulation of gene expression was disturbed in the retina. Remarkably, elimination of clock function by Bmal1-deficiency mitigates the progression of pathophysiology of the diabetic retina. Thus high-fat diet was seen to induce histopathology and molecular markers associated with diabetic retinopathy in wild type but not in Bmal1-deficient mice. The data of the present study suggest that Bmal1/the retinal clock system is both, a target and an effector of diabetes mellitus in the retina and hence represents a putative therapeutic target in the pathogenesis of diabetic retinopathy.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2021-10-01 | Experimental eye research |