Evidence map›Paper›PMID 42751196›Full record

ReviewGenes & diseases2027

Lactylation: Metabolic epigenetic regulation and cell death mechanisms in myocardial ischemia‒reperfusion injury.

Xiaoting Yang, Hui Wu, Di Liu, Gang Zhou, Dong Zhang, Yanfang Liu, Yi Li, Tian Zhou, Yan Xiong

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Genes & diseases, 2027. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Xiaoting YangDepartment of Cardiology, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, Hubei 443000, China.
Hui WuDepartment of Cardiology, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, Hubei 443000, China.
Di LiuDepartment of Cardiology, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Huangshi, Hubei 435000, China.
Gang ZhouDepartment of Cardiology, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, Hubei 443000, China.
Dong ZhangDepartment of Cardiology, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, Hubei 443000, China.
Yanfang LiuDepartment of Cardiology, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, Hubei 443000, China.
Yi LiDepartment of Cardiology, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, Hubei 443000, China.
Tian ZhouDepartment of Cardiology, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, Hubei 443000, China.
Yan XiongDepartment of Cardiology, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, Hubei 443000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One important pathogenic process that contributes to subsequent damage after myocardial infarction (MI) revascularization is myocardial ischemia/reperfusion injury (MI/RI). Its underlying mechanisms are controlled by traditional post-translational modifications (PTMs) like acetylation, methylation, phosphorylation, and ubiquitination, and involve several cell death pathways, such as autophagy, apoptosis, pyroptosis, and ferroptosis. Histone lysine lactylation (Kla), a novel metabolically related epigenetic regulation mechanism, has attracted a lot of attention in recent years. This review systematically clarifies the crucial role of lactate in cardiac energy metabolism and its influence on Kla modification, exploring Kla's dual regulatory function in MI/RI. It demonstrates a significant interaction between Kla and changes like acetylation, phosphorylation, N6-methyladenosine (m6A) methylation, and ubiquitination, thereby establishing putative connections that regulate cell death in MI/RI. Targeting lactate-related molecules such as lactate dehydrogenase A (LDHA), monocarboxylate transporters (MCTs), and histone deacetylases (HDACs) shows therapeutic potential. Therefore, targeted intervention molecules applicable at different stages of MI/RI are explored. Ultimately, elucidating the dynamic patterns of Kla and its crucial involvement in various biological processes will create new paradigms and potential therapeutic targets for the prevention and treatment of MI/RI.

Indexed as

ApoptosisAutophagyFerroptosisLactate metabolismLactationMyocardial ischemia/reperfusion injuryPosttranslational modificationsPyroptosis

Identifiers

PMID42751196
PMCPMC13579291

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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.