ArticleAging cell2026
Endothelial Sirtuins and Mitochondrial Function Are Associated With Testosterone Status: Implications for Accelerated Vascular Aging in Middle-Age and Older Men With Low Testosterone.
Article in Aging cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Chasing the FoxO in Metabolic Disorders: Novel Considerations for Oxidative Stress, Programmed Cell Death, Wnt, and the Gut Microbiome.Antioxidants (Basel, Switzerland) · 2026Review
- Running out the clock: Circadian rhythm dysfunction in cognitive disease.International review of neurobiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
Middle-aged/older (MA/O) men with low testosterone have greater oxidative stress-mediated vascular endothelial dysfunction, a major risk factor for cardiovascular disease (CVD). Testosterone deficiency impairs mitochondria, a source and target of oxidative stress. Whether the greater vascular endothelial dysfunction in MA/O men with low testosterone is related to mitochondrial dysfunction is unknown. This cross-sectional study measured mitochondrial respiration in peripheral blood mononuclear cells (PBMCs), and regulators of mitochondrial function (i.e., sirtuins [SIRTs]), and oxidant burden in vascular endothelial cells from (1) young adult men with normal testosterone (18-40 years; serum testosterone ≥ 13.9 nmol/L [400 ng/dL]; n = 23); (2) MA/O men with normal testosterone (50-75 years; serum testosterone ≥ 13.9 nmol/L [400 ng/dL]; n = 57), and (3) MA/O men with low testosterone (50-75 years; serum testosterone < 10.4 nmol/L [300 ng/dL]; n = 21). PBMCs from MA/O men with low testosterone had reduced carbohydrate (2.96 ± 0.65 vs. 6.85 ± 0.77 pmol/s·million cells; p = 0.001) and lipid-supported (4.10 ± 0.67 vs. 6.23 ± 0.69 pmol/s·million cells; p = 0.047) state 2 respiration compared to young men, and lower carbohydrate-supported uncoupled respiration than age-matched men with normal testosterone (17.77 ± 2.91 vs. 24.9 ± 1.93 pmol/s·million cells; p = 0.046). SIRT3 arterial (0.64 ± 0.04 vs. 0.99 ± 0.08 FU; p = 0.003) and venous (0.61 ± 0.03 vs. 0.92 ± 0.07 FU; p = 0.003) expression was lower in endothelial cells from MA/O men with low testosterone compared to age-matched men with normal testosterone. This study highlights the potential role of mitochondrial respiration and regulation in accelerated vascular aging in hypogonadal MA/O men. Importantly, these findings provide promising evidence for clinical therapeutic interventions to target mitochondrial health and SIRT3 to mitigate accelerated vascular aging in hypogonadal MA/O men.
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