Evidence map›Paper›PMID 36964992›Full record

ArticleAging cell2023

Transcriptional activation of endogenous Oct4 via the CRISPR/dCas9 activator ameliorates Hutchinson-Gilford progeria syndrome in mice.

Junyeop Kim, Yerim Hwang, Sumin Kim, Yujung Chang, Yunkyung Kim, Youngeun Kwon, Jongpil Kim

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.9field-weighted citation impact, top 9% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Advances and clinical potential of epigenome editing.Cellular and molecular life sciences : CMLS · 2026
    Review
  2. Epigenetic editing: from concept to clinic.Nature reviews. Drug discovery · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Epigenetic Dynamics in Reprogramming to Dopaminergic Neurons for Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  10. Review
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Junyeop KimLaboratory of Stem Cells & Cell reprogramming, Department of Chemistry, Dongguk University, 100-715, Seoul, Korea.
Yerim HwangLaboratory of Stem Cells & Cell reprogramming, Department of Chemistry, Dongguk University, 100-715, Seoul, Korea.
Sumin KimLaboratory of Stem Cells & Cell reprogramming, Department of Chemistry, Dongguk University, 100-715, Seoul, Korea.
Yujung ChangLaboratory of Stem Cells & Cell reprogramming, Department of Chemistry, Dongguk University, 100-715, Seoul, Korea.
Yunkyung KimLaboratory of Stem Cells & Cell reprogramming, Department of Chemistry, Dongguk University, 100-715, Seoul, Korea.
Youngeun KwonLaboratory of Protein Engineering, Department of Biomedical Engineering, Dongguk University, 04620, Seoul, Korea.
Jongpil KimLaboratory of Stem Cells & Cell reprogramming, Department of Chemistry, Dongguk University, 100-715, Seoul, Korea.ORCID 0000-0003-3876-6020
Dongguk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Partial cellular reprogramming via transient expression of Oct4, Sox2, Klf4, and c-Myc induces rejuvenation and reduces aged-cell phenotypes. In this study, we found that transcriptional activation of the endogenous Oct4 gene by using the CRISPR/dCas9 activator system can efficiently ameliorate hallmarks of aging in a mouse model of Hutchinson-Gilford progeria syndrome (HGPS). We observed that the dCas9-Oct4 activator induced epigenetic remodeling, as evidenced by increased H3K9me3 and decreased H4K20me3 levels, without tumorization. Moreover, the progerin accumulation in HGPS aorta was significantly suppressed by the dCas9 activator-mediated Oct4 induction. Importantly, CRISPR/dCas9-activated Oct4 expression rescued the HGPS-associated vascular pathological features and lifespan shortening in the mouse model. These results suggest that partial rejuvenation via CRISPR/dCas9-mediated Oct4 activation can be used as a novel strategy in treating geriatric diseases.

Indexed as

ProgeriaAgingAnimalsCellular ReprogrammingClustered Regularly Interspaced Short Palindromic RepeatsDisease Models, AnimalLamin Type AMiceTranscriptional ActivationLamin Type AagingCRISPR/dCas9Hutchinson-Gilford progeria syndromeOct4rejuvenation

Identifiers

PMID36964992
PMCPMC10265166
OpenAlexW4360951902

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.