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Related Concept Videos

Diabetic Retinopathy01:27

Diabetic Retinopathy

DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...

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Related Experiment Video

Updated: May 21, 2026

LipidUNet-Machine Learning-Based Method of Characterization and Quantification of Lipid Deposits Using iPSC-Derived Retinal Pigment Epithelium
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Published on: July 28, 2023

Adipocytes influence choroidal neovascularization via PRDM16.

Roberto Diaz-Marin1, Masayuki Hata1, Vera Guber2

  • 1Department of Biochemistry, Maisonneuve-Rosemont Hospital Research Centre, Université de Montréal, Montréal, QC, Canada.

EMBO Molecular Medicine
|May 19, 2026
PubMed
Summary
This summary is machine-generated.

Adipose tissue, specifically adipocytes expressing Prdm16, exacerbates neovascular age-related macular degeneration (nAMD). Targeting these adipocytes may offer new therapeutic strategies for this common cause of blindness.

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Area of Science:

  • Ophthalmology
  • Metabolism
  • Molecular Biology

Background:

  • Neovascular age-related macular degeneration (nAMD) is a leading cause of vision loss in older adults, characterized by abnormal blood vessel growth (choroidal neovascularization - CNV).
  • While genetics and age are risk factors, modifiable factors like body adiposity are increasingly implicated in AMD pathogenesis.
  • The precise mechanisms linking adipose tissue to nAMD remain incompletely understood.

Purpose of the Study:

  • To investigate the role of adipose tissue (AT), particularly adipocyte-specific pathways, in exacerbating CNV in a mouse model of nAMD.
  • To identify specific molecular mediators within adipocytes that contribute to pathological angiogenesis in nAMD.

Main Methods:

  • Laser-induced CNV model in mice to mimic nAMD.
  • Analysis of gene expression changes in distal inguinal white AT (iWAT) following retinal injury.
  • Selective deletion and reintroduction of the transcription factor Prdm16 in adipocytes.
  • Ex vivo experimentation to assess theSecretory function of adipocytes.

Main Results:

  • Laser-induced CNV upregulated browning and inflammatory genes in iWAT.
  • Selective deletion of Prdm16 in adipocytes reduced AT browning and significantly inhibited CNV.
  • Reintroducing Prdm16-expressing AT aggravated CNV in Prdm16-deficient mice.
  • Prdm16-expressing adipocytes secreted angiogenic factors like IGFBP5, promoting pathological angiogenesis.

Conclusions:

  • Prdm16-expressing adipocytes play a critical role in promoting CNV, a key feature of nAMD.
  • This study highlights a novel communication pathway between distal adipose tissue and the retina in the pathogenesis of AMD.
  • Targeting Prdm16 in adipocytes presents a potential therapeutic avenue for nAMD.