Evidence map›Paper›PMID 39205384›Full record

ArticleJournal of cellular and molecular medicine2024

Lactate regulates pathological cardiac hypertrophy via histone lactylation modification.

Shuai-Shuai Zhao, Jinlong Liu, Qi-Cai Wu, Xue-Liang Zhou

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed.

  1. Review
  2. Lactate-Mediated Lysine Lactylation in Renal Fibrosis: Current Progress and Challenges.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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.

Shuai-Shuai ZhaoDepartment of Cardiac Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Jinlong LiuInstitute of Translational Medicine, Shanghai University, Shanghai, China.
Qi-Cai WuDepartment of Cardiac Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Xue-Liang ZhouDepartment of Cardiac Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.ORCID 0009-0000-8678-9839

Funding

National Natural Science Foundation of China 81970199National Natural Science Foundation of China 82070303National Natural Science Foundation of China 82160082National Natural Science Foundation of China 82360060Natural Science Foundation of Jiangxi Province 20202BAB206006Natural Science Foundation of Jiangxi Province 20232ACB206003Natural Science Foundation of Jiangxi Province 20232BAB206113
6 · The paper itself

Abstract

Under the long-term pressure overload stimulation, the heart experiences embryonic gene activation, leading to myocardial hypertrophy and ventricular remodelling, which can ultimately result in the development of heart failure. Identifying effective therapeutic targets is crucial for the prevention and treatment of myocardial hypertrophy. Histone lysine lactylation (HKla) is a novel post-translational modification that connects cellular metabolism with epigenetic regulation. However, the specific role of HKla in pathological cardiac hypertrophy remains unclear. Our study aims to investigate whether HKla modification plays a pathogenic role in the development of cardiac hypertrophy. The results demonstrate significant expression of HKla in cardiomyocytes derived from an animal model of cardiac hypertrophy induced by transverse aortic constriction surgery, and in neonatal mouse cardiomyocytes stimulated by Ang II. Furthermore, research indicates that HKla is influenced by glucose metabolism and lactate generation, exhibiting significant phenotypic variability in response to various environmental stimuli. In vitro experiments reveal that exogenous lactate and glucose can upregulate the expression of HKla and promote cardiac hypertrophy. Conversely, inhibition of lactate production using glycolysis inhibitor (2-DG), LDH inhibitor (oxamate) and LDHA inhibitor (GNE-140) reduces HKla levels and inhibits the development of cardiac hypertrophy. Collectively, these findings establish a pivotal role for H3K18la in pathological cardiac hypertrophy, offering a novel target for the treatment of this condition.

Indexed as

CardiomegalyHistonesLactic AcidMyocytes, CardiacAnimalsDisease Models, AnimalGlucoseGlycolysisLysineMaleMiceMice, Inbred C57BLProtein Processing, Post-TranslationalGlucoseHistonesLactic AcidLysinecardiac hypertrophyH3K18lahistone lysine lactylationHKlapost‐translational modification

Identifiers

PMID39205384
PMCPMC11358213

What Socratic 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 Socratic graph.