Evidence map›Paper›PMID 35571189›Full record

ArticleFrontiers in cardiovascular medicine2022

KDM3A Inhibition Ameliorates Hyperglycemia-Mediated Myocardial Injury by Epigenetic Modulation of Nuclear Factor Kappa-B/P65.

Bofang Zhang, Jing Zhang, Gen Liu, Xin Guo, Xiaopei Liu, Jing Chen

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 16% of its field
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

9 citing papers in PubMed, 11 citations in OpenAlex.

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  7. Histone demethylases in autophagy and inflammation.Cell communication and signaling : CCS · 2025
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Bofang ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute, Wuhan University, Wuhan, China.
Jing ZhangDepartment of Cardiology, The First College of Clinical Medical Science, Yichang Central People's Hospital, China Three Gorges University, Yichang, China.
Gen LiuDepartment of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute, Wuhan University, Wuhan, China.
Xin GuoDepartment of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute, Wuhan University, Wuhan, China.
Xiaopei LiuDepartment of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute, Wuhan University, Wuhan, China.
Jing ChenDepartment of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute, Wuhan University, Wuhan, China.
Renmin Hospital of Wuhan University · CNChina Three Gorges University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: Even after the glucose level returns to normal, hyperglycemia-induced cardiac dysfunction as well as reactive oxygen species (ROS) generation, inflammatory responses, and apoptosis continued deterioration, showing a long-lasting adverse effect on cardiac function and structure. We aimed to unveil the molecular and cellular mechanisms underlying hyperglycemia-induced persistent myocardial injury and cardiac dysfunction. Methods and Results: Recently, the accumulated evidence indicated epigenetic regulation act as a determining factor in hyperglycemia-induced continuous cardiovascular dysfunction. As an important histone demethylase, the expression of lysine-specific demethylase 3A (KDM3A) was continually increased, accompanied by a sustained decline of H3K9me2 levels in diabetic myocardium even if received hypoglycemic therapy. Besides, by utilizing gain- and loss-of-functional approaches, we identified KDM3A as a novel regulator that accelerates hyperglycemia-mediated myocardial injury by promoting ROS generation, aggregating inflammatory reaction, and facilitating cell apoptosis Conclusion: This study revealed histone-modifying enzymes KDM3A drives persistent oxidative stress, inflammation, apoptosis, and subsequent myocardial injury in the diabetic heart by regulating the transcription of NF-κB/P65.

Indexed as

cardiac dysfunctionepigenetic regulationhyperglycemiaKDM3ANF-κB/p65

Identifiers

PMID35571189
PMCPMC9106140
OpenAlexW4225153288

What OpenQuestion holds

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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 OpenQuestion graph.