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@ARTICLE{Denk:305613,
author = {D. Denk and A. Singh and H. G. Kasler and D. D'Amico and J.
Rey and L. Alcober-Boquet and J. M. Gorol and C. Steup and
R. Tiwari and R. Kwok and R. J. Argüello and J. Faitg and
K. Sprinzl and S. Zeuzem$^*$ and V. Nekljudova and S. Loibl
and E. Verdin and C. Rinsch and F. R. Greten$^*$},
title = {{E}ffect of the mitophagy inducer urolithin {A} on
age-related immune decline: a randomized, placebo-controlled
trial.},
journal = {Nature aging},
volume = {5},
number = {11},
issn = {2662-8465},
address = {London},
publisher = {Nature Research},
reportid = {DKFZ-2025-02263},
pages = {2309-2322},
year = {2025},
note = {2025 Nov;5(11):2309-2322},
abstract = {Mitochondrial dysfunction and stem cell exhaustion
contribute to age-related immune decline, yet clinical
interventions targeting immune aging are lacking. Recently,
we demonstrated that urolithin A (UA), a mitophagy inducer,
expands T memory stem cells (TSCM) and naive T cells in
mice. In this randomized, double-blind, placebo-controlled
trial, 50 healthy middle-aged adults received oral UA (1,000
mg day-1) or placebo for 4 weeks; time points of analysis
were baseline and day 28. Primary outcomes were phenotypical
changes in peripheral CD3+ T cell subsets and immune
metabolic remodeling. UA expanded peripheral naive-like,
less terminally exhausted CD8+ cells (treatment difference
0.50 percentage points; $95\%$ CI = 0.16 to 0.83; P =
0.0437) while also increasing CD8+ fatty acid oxidation
capacity (treatment difference = 14.72 percentage points;
$95\%$ confidence interval (CI) = 6.46 to 22.99; P =
0.0061). Secondary outcomes included changes in plasma
cytokine levels (IL-6, TNF, IL-1β, IL-10), immune
populations assessed via flow cytometry, immune cell
function, and mitochondrial content. Analysis revealed
augmented mitochondrial biogenesis in CD8+ cells, increased
peripheral CD56dimCD16bright NK cells, and nonclassical
CD14loCD16hi monocytes in UA-treated participants, as well
as improved activation-elicited TNF secretion in T cells and
bacterial uptake by monocytes. Exploratory single-cell RNA
sequencing demonstrated UA-driven transcriptional shifts
across immune populations, modulating pathways linked to
inflammation and metabolism. These findings indicate that
short-term UA supplementation modulates human immune cell
composition and function, supporting its potential to
counteract age-related immune decline and inflammaging.
ClinicalTrials.gov registration number: NCT05735886 .},
cin = {FM01},
ddc = {610},
cid = {I:(DE-He78)FM01-20160331},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:41174221},
doi = {10.1038/s43587-025-00996-x},
url = {https://inrepo02.dkfz.de/record/305613},
}