ArticleAging cell2025
Longevity Humans Have Youthful Erythrocyte Function and Metabolic Signatures.
Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Ubiquitinated proteomics reveals potential epigenetic-energy metabolism mechanisms in senescent ovarian granulosa cells of advanced maternal age.Journal of assisted reproduction and genetics · 2026Article
- Towards Metabolomics-Guided Healthy and Anti-Aging Nutrition.Metabolites · 2026Article
- Inosine promotes erythrocyte metabolic reprogramming and restores oxygen release for rejuvenation via 2,3-BPG-PNP axis.Cell discovery · 2026Article
- Methyl eugenol attenuates age-associated oxidative fragility by coupling CaFrontiers in physiology · 2026Article
- Hemoglobin and human longevity: integrating oxygen transport, redox biology, and aging pathways - a narrative review.Annals of medicine and surgery (2012) · 2026Review
- Variations in Innate Immune Cell Subtypes Correlate with Epigenetic Clocks, Inflammaging and Health Outcomes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Red Blood Cells and Human Aging: Exploring Their Biomarker Potential.Diagnostics (Basel, Switzerland) · 2025Review
- Lysine Carboxymethyl Cysteinate, as a Topical Glutathione Precursor, Protects Against Oxidative Stress and UVB Radiation-Induced Skin Damage.Antioxidants (Basel, Switzerland) · 2025Article
- Life destiny of erythrocyte in high altitude erythrocytosis: mechanisms underlying the progression from physiological (moderate) to pathological (excessive) high-altitude erythrocytosis.Frontiers in genetics · 2025Review
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Longevity individuals have lower susceptibility to chronic hypoxia, inflammation, oxidative stress, and aging-related diseases. It has long been speculated that "rejuvenation molecules" exist in their blood to promote extended lifespan. We unexpectedly discovered that longevity individuals exhibit erythrocyte oxygen release function similar to young individuals, whereas most elderly show reduced oxygen release capacity. Untargeted erythrocyte metabolomics profiling revealed that longevity individuals are characterized by youth-like metabolic reprogramming and these metabolites effectively differentiate the longevity from the elderly. Quantification analyses led us to identify multiple novel longevity-related metabolites within erythrocytes including adenosine, sphingosine-1-phosphate (S1P), and glutathione (GSH) related amino acids. Mechanistically, we revealed that increased bisphosphoglycerate mutase (BPGM) and reduced MFSD2B protein levels in the erythrocytes of longevity individuals collaboratively work together to induce elevation of intracellular S1P, promote the release of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) from membrane to the cytosol, and thereby orchestrate glucose metabolic reprogramming toward Rapoport-Luebering Shunt to induce the 2,3-BPG production and trigger oxygen delivery. Furthermore, increased glutamine and glutamate transporter expression coupled with the enhanced intracellular metabolism underlie the elevated GSH production and the higher anti-oxidative stress capacity in the erythrocytes of longevity individuals. As such, longevity individuals displayed less systemic hypoxia-related metabolites and more antioxidative and anti-inflammatory metabolites in the plasma, thereby healthier clinical outcomes including lower inflammation parameters as well as better glucose-lipid metabolism, and liver and kidney function. Overall, we identified that youthful erythrocyte function and metabolism enable longevity individuals to better counteract peripheral tissue hypoxia, inflammation, and oxidative stress, thus maintaining healthspan.
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