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

Changes in extracellular matrix cause RPE cells to make basal deposits and activate the alternative complement pathway.

Human molecular genetics - 1 Jan 2018

Fernandez-Godino Rosario, Bujakowska Kinga M, Pierce Eric A

Abstract excerpt

The design of efficient therapies for age-related macular degeneration (AMD) is limited by our understanding of the pathogenesis of basal deposits, which form between retinal pigment epithelium (RPE) and Bruch's membrane (BrM) early in disease, and involve activation of the complement system. To investigate the roles of BrM, RPE and complement in an AMD, we generated abnormal extracellular matrix (ECM) using...

Read the complete abstract on PubMed

Topics

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

Share to Cells, Cultured
Share to Complement C3
Share to Complement Pathway, Alternative

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Extracellular Matrix

Share to Extracellular Matrix Proteins

Share to Macular Degeneration

Share to Retinal Pigment Epithelium

Source

Open in PubMed Open full text

Identifiers

PMID: 29095988
DOI: 10.1093/hmg/ddx392
PMCID: PMC6251553

Genes

RPE
EFEMP1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Changes in extracellular matrix cause RPE cells to make basal deposits and activate the alternative complement pathway.PMID 29095988Read ↗

Changes in extracellular matrix cause RPE cells to make basal deposits and activate the alternative complement pathwaySemantic proximity Read ↗

A local complement response by RPE causes early-stage macular degeneration.Semantic proximity Read ↗

The R345W mutation in EFEMP1 is pathogenic and causes AMD-like deposits in miceSemantic proximity Read ↗

Mouse genetics and proteomic analyses demonstrate a critical role for complement in a model of DHRD/ML, an inherited macular degenerationSemantic proximity Read ↗

Complement C5 is Not Critical for the Formation of Sub-RPE Deposits in Efemp1 Mutant MiceSemantic proximity Read ↗

Complement C5 is not critical for the formation of sub-RPE deposits in Efemp1 mutant mice.Semantic proximity Read ↗

Complement C5 is not critical for the formation of sub-RPE deposits in <i>Efemp1</i> mutant miceSemantic proximity Read ↗

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

CR2-fH, A Targeted Inhibitor of Alternative Complement Pathway Reduces Dry AMD-Like Phenotype in AMD Patient iPSC-derived RPE Cells.Semantic proximity Read ↗

Formation and progression of sub-retinal pigment epithelium deposits in Efemp1 mutation knock-in mice: a model for the early pathogenic course of macular degenerationSemantic proximity Read ↗

Bruch’s Membrane Compartmentalizes Complement Regulation in the Eye with Implications for Therapeutic Design in Age-Related Macular DegenerationSemantic proximity Read ↗

As in Real Estate, Location Matters: Cellular Expression of Complement Varies Between Macular and Peripheral Regions of the Retina and Supporting TissuesSemantic proximity Read ↗

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