Evidence mapPaperPMID 39920549Full record

ReviewJournal of cardiovascular translational research2025

Targeting Lactic Acid Modification in Ischemic Heart Diseases: Novel Therapeutics and Mechanism.

Tangjiang Wan, Yucheng Liang, Tianwen Wei, Zijie Chen, Yafei Li

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of cardiovascular translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
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 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. c-Myc: an emerging participant in heart failure.Frontiers in cardiovascular medicine · 2026
    Review
  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

5 authors.

Tangjiang WanDepartment of Cardiology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, 215000, Jiangsu Province, China.
Yucheng LiangDepartment of Cardiology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, 215000, Jiangsu Province, China.
Tianwen WeiDepartment of Cardiovascular Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Zijie ChenDepartment of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases, Fudan University, Shanghai, China.
Yafei LiDepartment of Cardiology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, 215000, Jiangsu Province, China. dryafeili@njmu.edu.cn.ORCID 0000-0002-4549-1611

Funding

Innovative Research Group Project of the National Natural Science Foundation of China 82370287Jiangsu Commission of Health NO.M2022042Natural Science Foundation of Jiangsu Province No. BK20231204Science and Technology Program of Suzhou NO.SKY2022188
6 · The paper itself

Abstract

Ischemic heart disease (IHD), especially acute myocardial infarction (AMI), has a high mortality rate and poses a great threat to human health. When myocardial infarction occurs, the structure and function of the myocardium are significantly damaged, and its metabolisms switch from oxidative phosphorylation to glycolysis, producing lactate. Lactylation, as a newly discovered post-translational modification (PMT) in recent years, is involved in the regulation of gene expression, and cell proliferation. Emerging studies have revealed that lactate and lactylation modifications participate in inflammation and cardiac repair, and play an important role in cardiovascular diseases, such as myocardial infarction, myocardial fibrosis, and heart failure. Therefore, in this review, we discuss how glucose metabolism, glycolytic end-product lactate, and lactylation potentially interact with pathological processes, including inflammation, cardiac fibrosis, and heart failure. And targeting glycolysis and lactylation modification could provide a promising future for cardiovascular diseases.

Indexed as

Cardiovascular AgentsEnergy MetabolismGlycolysisLactic AcidMyocardial IschemiaMyocardiumProtein Processing, Post-TranslationalAnimalsFibrosisHumansMolecular Targeted TherapySignal TransductionCardiovascular AgentsLactic AcidCardiovascular diseaseLactateLactylationMetabolismMyocardial infarction

Identifiers

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.