Evidence map›Paper›PMID 39747742›Full record

ArticleCardiovascular drugs and therapy2026

Dexmedetomidine Inhibits Ferroptosis to Alleviate Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury by Regulating the HDAC2/FPN Pathway.

Yueqi Fu, QingDong Wang, DongWei Wang, Yicong Li

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Article in Cardiovascular drugs and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

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0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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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

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3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Yueqi FuJiamusi University, Jiamusi, 154002, Heilongjiang Province, China.
QingDong WangDepartment of Anesthesiology, The First Affiliated Hospital of Jiamusi University, No.348 Dexiang Street, Xiangyang District, Jiamusi, 154002, Heilongjiang Province, China.
DongWei WangDepartment of Anesthesiology, The First Affiliated Hospital of Jiamusi University, No.348 Dexiang Street, Xiangyang District, Jiamusi, 154002, Heilongjiang Province, China. mhnhua@163.com.
Yicong LiDepartment of Anesthesiology, Hainan Hosiptal of Chinese PLA General Hospital, No.80 Jianglin Street, Haitang District, Sanya City, Hainan Province, China. liyicong2000@163.com.ORCID 0009-0004-0499-7765

Funding

Basic scientific research funds for colleges and universities in Heilongjiang Province 2023-KYYWF-0602
6 · The paper itself

Abstract

purposeMyocardial ischemia/reperfusion injury (MIRI) is closely associated with ferroptosis. Dexmedetomidine (Dex) has good therapeutic effects on MIRI. This study investigates whether dexmedetomidine (Dex) regulates ferroptosis during MIRI by affecting ferroportin1 (FPN) levels and elucidates the underlying mechanisms.

methodsA murine MIRI model was established using male C57BL/6 J mice subjected to 30 min of left anterior descending coronary artery ligation followed by 48 h of reperfusion. In vitro, cardiomyocyte hypoxia/reoxygenation (H/R) models were created with 16 h of hypoxia and 8 h of reoxygenation. Triphenyltetrazolium chloride (TTC) staining was employed to determine infarct size. The pathological changes in myocardial tissues were assessed using hematoxylin-eosin (HE) staining. Lipid reactive oxygen species (ROS) level was detected using BODIPY™ 581/591 C11, and ferrous iron (Fe

resultsDex alleviated ferroptosis in cardiomyocytes by upregulating FPN levels, which mitigated H/R-induced oxidative damage. FPN knockdown abolished the protective effects of Dex, confirming its dependence on FPN expression. Additionally, HDAC2 knockdown alleviated I/R-induced myocardial injury and ferroptosis in mice. Moreover, H/R-induced HDAC2 upregulation transcriptionally inhibited FPN expression by reducing the H3K27Ac level in the FPN promoter region, but Dex therapy restored this impact via inhibition of HDAC2. As expected, HDAC2 overexpression partially reversed the inhibitory effect of Dex on H/R-mediated cardiomyocyte ferroptosis.

conclusionDex alleviated H/R-mediated cardiomyocyte ferroptosis through regulating the HDAC2/FPN axis. Our findings lend theoretical support to the use of Dex in MIRI therapy.

Indexed as

DexmedetomidineFerroptosisHistone Deacetylase 2Myocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacAnimalsCell HypoxiaDisease Models, AnimalFerroportinMaleMiceMice, Inbred C57BLSignal TransductionDexmedetomidineFerroportinHdac2 protein, mouseHistone Deacetylase 2DexmedetomidineFerroptosisFPNHDAC2Myocardial ischemia/reperfusion injury

Identifiers

PMID39747742

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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.