Evidence map›Paper›PMID 41034497›Full record

ArticleNature biotechnology2026

Design of optimized epigenetic regulators for durable gene silencing with application to PCSK9 in nonhuman primates.

Shaoshuai Mao, Wenbo Peng, Zhengyan Feng, Yang Chen, Jing Sun, Haiting Chen, Pengcheng Wang, Pinzheng Huang, Junzheng Zhao, Leilei Wu and 13 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Advances and clinical potential of epigenome editing.Cellular and molecular life sciences : CMLS · 2026
    Review
  4. Article
  5. Article
  6. Review
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

23 authors.

Shaoshuai Mao *Epigenic Therapeutics, Inc., Shanghai, China.ORCID http://orcid.org/0009-0001-8130-1985
Wenbo Peng *Epigenic Therapeutics, Inc., Shanghai, China.
Zhengyan Feng *Epigenic Therapeutics, Inc., Shanghai, China.
Yang Chen *Epigenic Therapeutics, Inc., Shanghai, China.
Jing Sun *Epigenic Therapeutics, Inc., Shanghai, China.
Haiting Chen *Department of Cardiology, National Cardiovascular Disease Regional Center for Anhui, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Pengcheng WangEpigenic Therapeutics, Inc., Shanghai, China.
Pinzheng HuangEpigenic Therapeutics, Inc., Shanghai, China.ORCID http://orcid.org/0009-0003-5946-4053
Junzheng ZhaoEpigenic Therapeutics, Inc., Shanghai, China.
Leilei WuEpigenic Therapeutics, Inc., Shanghai, China.
Yifan WangEpigenic Therapeutics, Inc., Shanghai, China.
Junjian LiuEpigenic Therapeutics, Inc., Shanghai, China.
Hao LuoEpigenic Therapeutics, Inc., Shanghai, China.
Ying ZangEpigenic Therapeutics, Inc., Shanghai, China.
Changqing YangEpigenic Therapeutics, Inc., Shanghai, China.
Xue QiaoEpigenic Therapeutics, Inc., Shanghai, China.
Zhiwei LuEpigenic Therapeutics, Inc., Shanghai, China.
Hongjun WuEpigenic Therapeutics, Inc., Shanghai, China.
Mingjie ChenEpigenic Therapeutics, Inc., Shanghai, China.
Di SunEpigenic Therapeutics, Inc., Shanghai, China.
Jun XieDepartment of Cardiology, National Cardiovascular Disease Regional Center for Anhui, The First Affiliated Hospital of Anhui Medical University, Hefei, China. xiejun@ahmu.edu.cn.
Yidi SunInstitute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, State Key Laboratory of Genetic Evolution and Animal Models, Chinese Academy of Sciences, Shanghai, China. ydsun@ion.ac.cn.ORCID http://orcid.org/0000-0002-4191-2917
Changyang ZhouInstitute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, State Key Laboratory of Genetic Evolution and Animal Models, Chinese Academy of Sciences, Shanghai, China. zhouchangyang@ion.ac.cn.ORCID http://orcid.org/0000-0002-3012-1001

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic editing is a promising strategy for modifying gene expression while avoiding the permanent alterations and potential genotoxicity of genome-editing technologies. Here we designed optimized epigenetic regulators (EpiRegs) by testing combinations of transcription activator-like effector (TALE)-based and catalytically deactivated Cas9 (dCas9)-based epigenetic modification effectors and fusion protein structures. TALE-based EpiReg (EpiReg-T) achieved a final efficiency of 98% in mice, surpassing the initial dCas9-based efficiency of 64%. We demonstrated the approach in macaques by introducing DNA methylation and histone modifications to inhibit proprotein convertase subtilisin/kexin type 9 (PCSK9) expression, thereby lowering low-density lipoprotein cholesterol levels. A single dose of EpiReg-T delivered with lipid nanoparticles achieved efficient (>90%) and long-lasting (343 days) silencing of PCSK9 in the liver. Integrative multiomic analyses revealed minimal off-target effects in EpiReg-T-treated monkeys, mice and human-derived cells. EpiReg can be redirected to other genes by reengineering the DNA-binding domain. Our findings represent a step toward the clinical application of epigenetic editing for the treatment of human diseases.

Indexed as

Epigenesis, GeneticGene SilencingProprotein Convertase 9AnimalsDNA MethylationEpigenome EditingGene EditingHumansMiceProprotein Convertase 9

Identifiers

PMID41034497

What Socratic holds

Textmetadata
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 Socratic graph.