Evidence map›Paper›PMID 39349670›Full record

ArticleCommunications biology2024

Cpt1a Drives primed-to-naïve pluripotency transition through lipid remodeling.

Zhaoyi Ma, Xingnan Huang, Junqi Kuang, Qiannan Wang, Yue Qin, Tao Huang, Zechuan Liang, Wei Li, Yu Fu, Pengli Li and 7 more

Abstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

17 authors.

Zhaoyi Ma *College of Life Sciences, Zhejiang University, Hangzhou, China.
Xingnan Huang *Laboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Junqi KuangLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Qiannan WangLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Yue QinLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Tao HuangCollege of Life Sciences, Zhejiang University, Hangzhou, China.
Zechuan LiangCollege of Life Sciences, Zhejiang University, Hangzhou, China.
Wei LiLaboratory on Stem Cell and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Yu FuLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Pengli LiLaboratory on Stem Cell and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Yixin FanLaboratory on Stem Cell and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Ziwei ZhaiLaboratory on Stem Cell and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Xiaomin WangLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Jin MingLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Chengchen ZhaoLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.ORCID 0000-0002-8454-6347
Bo WangLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.ORCID 0000-0003-1182-952X
Duanqing PeiLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China. peiduanqing@westlake.edu.cn.ORCID 0000-0002-5222-014X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32300639National Natural Science Foundation of China (National Science Foundation of China) 32300672National Natural Science Foundation of China (National Science Foundation of China) 92068201
6 · The paper itself

Abstract

Metabolism has been implicated in cell fate determination, particularly through epigenetic modifications. Similarly, lipid remodeling also plays a role in regulating cell fate. Here, we present comprehensive lipidomics analysis during BMP4-driven primed to naive pluripotency transition or BiPNT and demonstrate that lipid remodeling plays an essential role. We further identify Cpt1a as a rate-limiting factor in BiPNT, driving lipid remodeling and metabolic reprogramming while simultaneously increasing intracellular acetyl-CoA levels and enhancing H3K27ac at chromatin open sites. Perturbation of BiPNT by histone acetylation inhibitors suppresses lipid remodeling and pluripotency transition. Together, our study suggests that lipid remodeling promotes pluripotency transitions and further regulates cell fate decisions, implicating Cpt1a as a critical regulator between primed-naive cell fate control.

Indexed as

Carnitine O-PalmitoyltransferaseLipid MetabolismAnimalsCell DifferentiationCellular ReprogrammingLipidomicsMicePluripotent Stem CellsCarnitine O-PalmitoyltransferaseCPT1B protein, mouse

Identifiers

PMID39349670
PMCPMC11442460

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.