| First Author | Zhang E | Year | 2020 |
| Journal | Mamm Genome | Volume | 31 |
| Issue | 3-4 | Pages | 77-85 |
| PubMed ID | 32342224 | Mgi Jnum | J:300802 |
| Mgi Id | MGI:6504101 | Doi | 10.1007/s00335-020-09837-1 |
| Citation | Zhang E, et al. (2020) PKM2 ablation enhanced retinal function and survival in a preclinical model of retinitis pigmentosa. Mamm Genome 31(3-4):77-85 |
| abstractText | Retinitis pigmentosa (RP) is a neurodegenerative disorder that causes irreversible vision loss in over 1.5 million individuals world-wide. The genetic heterogeneity of RP necessitates a broad therapy that is able to provide treatment in a gene- and mutation- non-specific manner. In this study, we identify the therapeutic benefits of metabolic reprogramming by targeting pyruvate kinase M2 (PKM2) in a Pde6beta preclinical model of RP. The genetic contributions of PKM2 inhibition in retinal degeneration were evaluated through histology and electroretinogram (ERG) followed by a statistical analysis using a linear regression model. Notably, PKM2 ablation resulted in thicker retinal layers in Pde6beta-mutated mice as compared to the controls, suggesting greater photoreceptor survival. Consistent with these anatomical findings, ERG analyses revealed that the maximum b-wave is on average greater in Pkm2 knockout mice than in mice with intact Pkm2, indicating enhanced photoreceptor function. These rescue phenotypes from Pkm2 ablation in a preclinical model of RP indicate that a metabolome reprogramming may be useful in treating RP. |
