Evidence map›Paper›PMID 39467114›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Dexmedetomidine Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting MDH2 Lactylation via Regulating Metabolic Reprogramming.

Han She, Yi Hu, Guozhi Zhao, Yunxia Du, Yinyu Wu, Wei Chen, Yong Li, Yi Wang, Lei Tan, Yuanqun Zhou and 7 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing 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

78 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  17. [Lactate induces gastric mucosal injury by promoting M1 polarization of macrophagesNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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18 more citing papers are in PubMed but not listed here.

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.

Han SheDepartment of Anesthesiology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Yi HuDepartment of Anesthesiology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Guozhi ZhaoDepartment of Urology Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yunxia DuDepartment of Anesthesiology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Yinyu WuDepartment of Anesthesiology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Wei ChenDepartment of Anesthesiology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Yong LiDepartment of Anesthesiology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Yi WangDepartment of Anesthesiology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Lei TanDepartment of Anesthesiology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Yuanqun ZhouShock and Transfusion Department, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Jie ZhengDepartment of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Qinghui LiShock and Transfusion Department, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Hong YanDepartment of Anesthesiology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Qingxiang MaoDepartment of Anesthesiology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Deyu ZuoDepartment of Rehabilitation Medicine, The First Affiliated Hospital of Chongqing University of Chinese Medicine, Chongqing Traditional Chinese Medicine Hospital, Chongqing, 400021, China.
Liangming LiuShock and Transfusion Department, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Tao LiShock and Transfusion Department, Daping Hospital, Army Medical University, Chongqing, 400042, China.ORCID 0000-0002-8371-7060

Funding

Chongqing Medical Young Talents Program YXQN202415Chongqing Medical Young Talents Program YXQN202452Chongqing Natural Science Foundation Innovation and Development Joint Fund (Chongqing Education Commission) CSTB2024NSCQ- LZX0079Chongqing Talent Program: Innovative Leading Talents CSTC2024YCJH-BGZXM0011High-Level Military Technological Innovation Talent ProgramNational Natural Science Foundation of China 82270523National Natural Science Foundation of China 82300561National Natural Science Foundation of China 82305006Natural Science Foundation of Chongqing CSTB2023NSCQ-MSX0713Sprint Program of Joint Medical Research of Chongqing Science and Chongqing Health Commission
6 · The paper itself

Abstract

Myocardial ischemia-reperfusion injury (MIRI) significantly worsens the outcomes of patients with cardiovascular diseases. Dexmedetomidine (Dex) is recognized for its cardioprotective properties, but the related mechanisms, especially regarding metabolic reprogramming, have not been fully clarified. A total of 60 patients with heart valve disease are randomly assigned to Dex or control group. Blood samples are collected to analyze cardiac injury biomarkers and metabolomics. In vivo and vitro rat models of MIRI are utilized to assess the effects of Dex on cardiac function, lactate production, and mitochondrial function. It is found that postoperative CK-MB and cTNT levels are significantly lower in the Dex group. Metabolomics reveals that Dex regulates metabolic reprogramming and reduces lactate level. In Dex-treated rats, the myocardial infarction area is reduced, and myocardial contractility is improved. Dex inhibits glycolysis, reduces lactate, and improves mitochondrial function following MIRI. Lactylation proteomics identifies that Dex reduces the lactylation of Malate Dehydrogenase 2(MDH2), thus alleviating myocardial injury. Further studies reveal that MDH2 lactylation induces ferroptosis, leading to MIRI by impairing mitochondrial function. Mechanistic analyses reveal that Dex upregulates Nuclear Receptor Subfamily 3 Group C Member 1(NR3C1) phosphorylation, downregulates Pyruvate Dehydrogenase Kinase 4 (PDK4), and reduces lactate production and MDH2 lactylation. These findings provide new therapeutic targets and mechanisms for the treatment for MIRI.

Indexed as

DexmedetomidineDisease Models, AnimalMyocardial Reperfusion InjuryAnimalsBiomarkersFemaleHumansMaleMetabolic ReprogrammingMiddle AgedRatsRats, Sprague-DawleyBiomarkersDexmedetomidinedexmedetomidineferroptosislactylationmetabolic reprogrammingmyocardial ischemia‐reperfusion injury

Identifiers

PMID39467114
PMCPMC11672254

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Registered trials

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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.