Evidence map›Paper›PMID 38456209›Full record

ReviewClinical and translational medicine2024

Histone lactylation bridges metabolic reprogramming and epigenetic rewiring in driving carcinogenesis: Oncometabolite fuels oncogenic transcription.

Yu Zhang, Hang Song, Meili Li, Peirong Lu

Open access · goldAbstract readReview
In one paragraph

Review in Clinical and translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
11.9field-weighted citation impact, top 1% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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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

4 authors at 3 institutions in 1 country.

Yu ZhangDepartment of Clinical Medicine, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Hang SongDepartment of Ophthalmology, Peking Union Medical College Hospital, Beijing, China.
Meili LiDepartment of Ophthalmology, Eye Disease Prevention and Treatment Institute of Xuzhou, The Affiliated Xuzhou Municipal Hospital of Xuzhou Medical University, Xuzhou First People's Hospital, Xuzhou, Jiangsu, China.
Peirong LuDepartment of Ophthalmology, The First Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0002-1423-1737
Xuzhou Medical College · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNSoochow University · CN

Funding

Science and Technology Program of Suzhou SKJY2021015Science and Technology Program of Suzhou SYSD2020048Suzhou Municipal Health Commission KJXW2020077
6 · The paper itself

Abstract

Heightened lactate production in cancer cells has been linked to various cellular mechanisms such as angiogenesis, hypoxia, macrophage polarisation and T-cell dysfunction. The lactate-induced lactylation of histone lysine residues is noteworthy, as it functions as an epigenetic modification that directly augments gene transcription from chromatin. This epigenetic modification originating from lactate effectively fosters a reliance on transcription, thereby expediting tumour progression and development. Herein, this review explores the correlation between histone lactylation and cancer characteristics, revealing histone lactylation as an innovative epigenetic process that enhances the vulnerability of cells to malignancy. Moreover, it is imperative to acknowledge the paramount importance of acknowledging innovative therapeutic methodologies for proficiently managing cancer by precisely targeting lactate signalling. This comprehensive review illuminates a crucial yet inadequately investigated aspect of histone lactylation, providing valuable insights into its clinical ramifications and prospective therapeutic interventions centred on lactylation.

Indexed as

HistonesMetabolic ReprogrammingCarcinogenesisEpigenesis, GeneticHumansLactic AcidHistonesLactic Acidcancerhistone lactylationmetabolic reprogramming

Identifiers

PMID38456209
PMCPMC10921234
OpenAlexW4392595221

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.