ArticleLife medicine2025
Heterochronic parabiosis alters the transcriptomic landscape to combat aging and aging-related diseases in aging-accelerated mice.
Article in Life medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Restoring the FOXO1 geroprotective pathway via seno-resistant mesenchymal progenitor cells alleviates primate epididymal aging.Protein & cell · 2026Article
- Single-nucleus interrogation of primate small intestinal aging reveals NCoR1 decline as a conserved feature that is reversed by metformin.Nature aging · 2026Article
- Blood as the mirror and modulator of aging: mechanistic insights and rejuvenation strategies.Experimental & molecular medicine · 2026Review
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Authors and funding
13 authors.
Funding
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Abstract
Aging is a multifactorial process involving a gradual decline in cellular and tissue functions, making it a major risk factor for aging-related degenerative diseases. In this study, we utilized the senescence-accelerated mouse prone 8 mice model, which mimics pathological characteristics of Alzheimer's disease, fatty liver disease, and cardiac fibrosis, to construct a heterochronic parabiosis model and systematically investigate the rejuvenating effects of heterochronic parabiosis on the brain, liver, and heart. Our findings revealed that heterochronic parabiosis promotes synaptic plasticity and neuronal communication, restores hepatocyte metabolic functions, and reduces chronic inflammation and fibrosis in the heart. Notably, heterochronic parabiosis significantly downregulates the expression of age-related disease risk genes. In addition, endothelial cells, as cell types directly exposed to the circulatory environment, demonstrated the highest sensitivity to heterochronic parabiosis across three organs, and exhibited significantly reduced inflammation after intervention, suggesting that they may play an early and central role in the rejuvenation process. Overall, our study increases the understanding of the molecular and cellular mechanisms of aging and its related diseases, highlights the multiorgan and multitarget potential of heterochronic parabiosis in delaying aging and mitigating aging-related diseases, and provides new therapeutic targets for achieving healthy aging.
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Registered trials
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