A metabolic perspective on eIF1A and eIF3B inhibition as a potential therapeutic strategy in psoriasis
- 1Medical University of Graz, Department of Dermatology and Venereology, Graz, Austria.
Abstract
Psoriasis is a chronic inflammatory skin disease marked by epidermal hyperplasia and distinct metabolic alterations. Here, we investigated the metabolic impact of targeting translation initiation factors by performing 1H NMR-based metabolomic profiling on polar skin extracts from imiquimod-induced (IMQ) and K5.TGF{beta}1 transgenic (TGF{beta}) mouse models treated with eIF1A or eIF3B siRNA. IMQ-treated skin demonstrated significant, human-like metabolic shifts, including depleted energy substrates (glucose, glycogen, 3-hydroxybutyrate) and elevated phospholipid/nucleotide markers, which correlated strongly with epidermal thickness. In contrast, TGF{beta} skin exhibited no broad baseline polar metabolome changes. eIF1A/eIF3B inhibition selectively attenuated IMQ-associated energy and phospholipid alterations without causing widespread metabolic disruption in TGF{beta} skin. Overall, eIF1A/eIF3B inhibition ameliorated psoriasis-like pathology and mitigated disease-associated metabolic demands in a context-dependent manner.
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BibTeX
@misc{bordag2026metabolic,
title = {{A metabolic perspective on eIF1A and eIF3B inhibition as a potential therapeutic strategy in psoriasis}},
author = {N. Bordag and B. M. R. Bourgeois and T. Madl and P. Wolf and N. Golob-Schwarzl},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.08.757342},
url = {https://www.biorxiv.org/content/10.64898/2026.10.08.757342v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - A metabolic perspective on eIF1A and eIF3B inhibition as a potential therapeutic strategy in psoriasis
AU - N. Bordag
AU - B. M. R. Bourgeois
AU - T. Madl
AU - P. Wolf
AU - N. Golob-Schwarzl
PY - 2026
DA - 2026/10/08
PB - bioRxiv
DO - 10.64898/2026.10.08.757342
UR - https://www.biorxiv.org/content/10.64898/2026.10.08.757342v1
AB - Psoriasis is a chronic inflammatory skin disease marked by epidermal hyperplasia and distinct metabolic alterations. Here, we investigated the metabolic impact of targeting translation initiation factors by performing 1H NMR-based metabolomic profiling on polar skin extracts from imiquimod-induced (IMQ) and K5.TGF{beta}1 transgenic (TGF{beta}) mouse models treated with eIF1A or eIF3B siRNA. IMQ-treated skin demonstrated significant, human-like metabolic shifts, including depleted energy substrates (glucose, glycogen, 3-hydroxybutyrate) and elevated phospholipid/nucleotide markers, which correlated strongly with epidermal thickness. In contrast, TGF{beta} skin exhibited no broad baseline polar metabolome changes. eIF1A/eIF3B inhibition selectively attenuated IMQ-associated energy and phospholipid alterations without causing widespread metabolic disruption in TGF{beta} skin. Overall, eIF1A/eIF3B inhibition ameliorated psoriasis-like pathology and mitigated disease-associated metabolic demands in a context-dependent manner.
ER -