ArticleCell2016
In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming.
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 522 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
522 citing papers in PubMed.
- Article
- Inhibiting Glutaminase Reverses Senescence-Associated Mitochondrial Dysfunction and Skeletal Muscle Decline.Aging cell · 2026Article
- mRNA Therapeutics for Skin Rejuvenation: From Aging Atlases to Clinical Translation.Experimental dermatology · 2026Review
- Review
- Functional rejuvenation of endothelial cell aging by transient reprogramming.Basic research in cardiology · 2026Article
- In Vivo Direct Reprogramming: Current Progress and Future Prospects from Mechanisms to Therapeutic Application.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- CRISPRa-identified transcription factors reprogram glioblastoma into dendritic cell-like cells to elicit systemic antitumor immunity.Cell reports. Medicine · 2026Article
- The Hallmarks of Aging: From Molecular Mechanisms to Clinical Translation.International journal of molecular sciences · 2026Review
- Aging Biology of Bone-to-Tendon Healing and the Epigenetic Clock: A Biological-Age Readout of Rotator Cuff Healing Capacity.Biomedicines · 2026Review
- The hallmarks of skeletal muscle health.Nature metabolism · 2026Review
- Rejuvenation of corticospinal neurons enhances rehabilitation-associated corticospinal tract axon sprouting and functional recovery post photothrombotic ischemic stroke in mice.Genes & diseases · 2026Article
- Induced pluripotent stem cells from discovery to translation.Nature medicine · 2026Review
- Pluripotency, differentiation, and reprogramming: 20 years of induced pluripotent stem cells.BMC biology · 2026Article
- Article
- Electromagnetic field‑inducible gene switch: a non‑invasive platform for remote spatiotemporal gene control.Signal transduction and targeted therapy · 2026Article
- Epigenetic Skeletal Muscle Memory: The Impact of Physical Activity on Aging and Post-Injury Regeneration.Genes · 2026Review
- Conserved Partial Reprogramming Effects on the Methylome.Epigenomes · 2026Article
- Extracellular vesicles and epigenetic aging clocks in tissue aging: an exosome-focused conceptual framework with a focus on skin.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026Review
- Revisiting Pluripotency Acquisition: A Unified Framework for Reprogramming Strategies.Development, growth & differentiation · 2026Review
- The Mechanistic Study of Melatonin Regulation of p16Ink4a and Oct4 in Anti-Cellular Senescence.Journal of cellular and molecular medicine · 2026Article
462 more citing papers are in PubMed but not listed here.
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Authors and funding
22 authors.
Funding
Abstract
Aging is the major risk factor for many human diseases. In vitro studies have demonstrated that cellular reprogramming to pluripotency reverses cellular age, but alteration of the aging process through reprogramming has not been directly demonstrated in vivo. Here, we report that partial reprogramming by short-term cyclic expression of Oct4, Sox2, Klf4, and c-Myc (OSKM) ameliorates cellular and physiological hallmarks of aging and prolongs lifespan in a mouse model of premature aging. Similarly, expression of OSKM in vivo improves recovery from metabolic disease and muscle injury in older wild-type mice. The amelioration of age-associated phenotypes by epigenetic remodeling during cellular reprogramming highlights the role of epigenetic dysregulation as a driver of mammalian aging. Establishing in vivo platforms to modulate age-associated epigenetic marks may provide further insights into the biology of aging.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.