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

mTOR Inhibition via Rapamycin Treatment Partially Reverts the Deficit in Energy Metabolism Caused by FH Loss in RPE Cells

3 Dec 2021

Abstract excerpt

Age-related macular degeneration (AMD) is a complex degenerative disease of the retina with multiple risk-modifying factors, including aging, genetics, and lifestyle choices. The combination of these factors leads to oxidative stress, inflammation, and metabolic failure in the retinal pigment epithelium (RPE) with subsequent degeneration of photoreceptors in the retina. The alternative complement pathway is...

Read the complete abstract on PubMed

Topics

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

Share to Complement system in diseases
Share to Retinal Development and Disorders
Share to Retinal Diseases and Treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 34943047
DOI: 10.3390/antiox10121944

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

mTOR Inhibition via Rapamycin Treatment Partially Reverts the Deficit in Energy Metabolism Caused by FH Loss in RPE CellsPMID 34943047Read ↗

mTOR inhibition <i>via</i> Rapamycin treatment partially reverts the deficit in energy metabolism caused by FH loss in RPE cellsSemantic proximity Read ↗

Loss of Complement Factor H impairs antioxidant capacity and energy metabolism of human RPE cellsSemantic proximity Read ↗

Non-canonical roles of CFH in retinal pigment epithelial cells revealed by dysfunctional rare CFH variantsSemantic proximity Read ↗

CFH Loss in Human RPE Cells Leads to Inflammation and Complement System Dysregulation via the NF-κB PathwaySemantic proximity Read ↗

The AKT2/SIRT5/TFEB pathway as a potential therapeutic target in atrophic AMDSemantic proximity Read ↗

<i>CFH</i> loss in human RPE cells leads to inflammation and complement system dysregulation <i>via</i> the NF-κB pathwaySemantic proximity Read ↗

Complement Factor H (Y402H) polymorphism for age-related macular degeneration alters retinal lipidsSemantic proximity Read ↗

Glucose-Sensing ChREBP Protein in the Pathogenesis of Diabetic RetinopathySemantic proximity Read ↗

The Complement Factor H (Y402H) risk polymorphism for age-related macular degeneration affects metabolism and response to oxidative stress in the retinal pigment epithelium.Semantic proximity Read ↗

Impaired Mitochondrial Function in iPSC-Retinal Pigment Epithelium with the Complement Factor H Polymorphism for Age-Related Macular DegenerationSemantic proximity Read ↗

FH loss in RPE cells causes retinal degeneration in a human RPE-porcine retinal explant co-culture modelSemantic proximity Read ↗

Reprogramming towards anabolism impedes degeneration in a preclinical model of retinitis pigmentosaSemantic proximity Read ↗

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