ArticleNature aging2023
In vivo reprogramming leads to premature death linked to hepatic and intestinal failure.
Article in Nature aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 47 citations in OpenAlex.
- Oxidative stress drives liver failure during in vivo partial reprogramming.Molecules and cells · 2026Article
- Harnessing Lessons from Gel-Based and Advanced Biomaterial Therapeutics to Enable Direct Cellular Reprogramming.Gels (Basel, Switzerland) · 2026Review
- Developing chemical reprogramming strategies of non-hepatocytes for liver regeneration.Journal of advanced research · 2026Review
- Marine Bioactives in Liver Aging: Mechanistic Insights and Translational Potential.Marine drugs · 2026Review
- Local delivery of OSK factors enables partial cellular reprogramming to mitigate osteoarthritis and cartilage fibrosis.Experimental & molecular medicine · 2026Article
- In Vivo Chemical Reprogramming Is Associated With a Toxic Accumulation of Lipid Droplets Hindering Rejuvenation.Aging cell · 2026Article
- The harmonies played by miR-302/367 cluster in pluripotency, reprogramming, and rejuvenation.Stem cells translational medicine · 2026Review
- Molecular time machines unleashed: small-molecule-driven reprogramming to reverse the senescence.Stem cells translational medicine · 2026Review
- Epigenetic aging and rejuvenation of the brain: drivers, consequences, and interventions.BMB reports · 2026Review
- Organ-Specific Dedifferentiation and Epigenetic Remodeling in In Vivo Reprogramming.Aging cell · 2025Review
- Gene therapy strategies for aging intervention.Cell insight · 2025Review
- Biomarkers of aging: from molecules and surrogates to physiology and function.Physiological reviews · 2025Review
- Cell-based regenerative and rejuvenation strategies for treating neurodegenerative diseases.Stem cell research & therapy · 2025Review
- Research ofRegenerative therapy · 2025Review
- Review
- Current advances and future prospects of cell reprogramming in progeroid syndromes.Frontiers in cell and developmental biology · 2025Article
- Toward precision longevity: aging interventions in the single-cell atlas era.Frontiers in aging · 2025Review
- The Quest for Eternal Youth: Hallmarks of Aging and Rejuvenating Therapeutic Strategies.Biomedicines · 2024Review
- Epistemic uncertainty challenges aging clock reliability in predicting rejuvenation effects.Aging cell · 2024Article
- A cellular identity crisis? Plasticity changes during aging and rejuvenation.Genes & development · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 3 institutions in 3 countries.
Funding
Abstract
The induction of cellular reprogramming via expression of the transcription factors Oct4, Sox2, Klf4 and c-Myc (OSKM) can drive dedifferentiation of somatic cells and ameliorate age-associated phenotypes in multiple tissues and organs. However, the benefits of long-term in vivo reprogramming are limited by detrimental side-effects. Here, using complementary genetic approaches, we demonstrated that continuous induction of the reprogramming factors in vivo leads to hepatic and intestinal dysfunction resulting in decreased body weight and contributing to premature death (within 1 week). By generating a transgenic reprogrammable mouse strain, avoiding OSKM expression in both liver and intestine, we reduced the early lethality and adverse effects associated with in vivo reprogramming and induced a decrease in organismal biological age. This reprogramming mouse strain, which allows longer-term continuous induction of OSKM with attenuated toxicity, can help better understand rejuvenation, regeneration and toxicity during in vivo reprogramming.
Indexed as
Identifiers
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.