Adipocytes influence choroidal neovascularization via PRDM16
Diaz-Marin R., Hata M., Guber V., De Guire V., Wilson AM., Crespo-Garcia S.
Animal Study, published in EMBO Mol Med (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- EMBO Mol Med (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 42156503
- PMCID
- PMC13269495
- DOI
- 10.1038/s44321-026-00441-5
Abstract (original English)
Neovascular age-related macular degeneration (nAMD) is a prominent cause of blindness in the elderly, characterized by pathological subretinal choroidal neovascularization (CNV). While age and genetics predispose to AMD, modifiable factors such as body adiposity are also thought to contribute. In a mouse model of nAMD, we identified a role for adipose tissue (AT) in exacerbating CNV, specifically pathways in adipocytes expressing Prdm16. Laser-induced CNV in the retina led to heightened expression of genes associated with browning and inflammation in distal inguinal white AT (iWAT). Selective deletion of the browning-associated transcription factor Prdm16 in adipocytes inhibited AT browning and reduced CNV. Reintroduction of Prdm16-expressing adipose tissue was sufficient to aggravate CNV in Prdm16-deficient mice. Ex vivo experimentation suggested that Prdm16-expressing adipocytes secrete angiogenic factors such as IGFBP5 and contribute to pathological angiogenesis. Thus, Prdm16-expressing adipocytes contribute to CNV, highlighting communication between the retina and distal tissues in the pathogenesis of AMD.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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