Evidence map›Paper›PMID 40217309›Full record

ArticleHereditas2025

Decoding mitochondrial stress genes in DCM: towards precision diagnosis and therapy.

Bingbing Zhu, Hai Cheng, Jiawei Li, Yangyang Hu, Xiaoning Ge

Abstract read
In one paragraph

Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Bingbing ZhuDepartment of Cardiology, Suzhou Kowloon Hospital, Shanghai Jiaotong University School of Medicine, Suzhou, Jiangsu Province, 215028, China.
Hai ChengDepartment of Cardiology, Suzhou Kowloon Hospital, Shanghai Jiaotong University School of Medicine, Suzhou, Jiangsu Province, 215028, China.
Jiawei LiDepartment of Cardiology, Suzhou Kowloon Hospital, Shanghai Jiaotong University School of Medicine, Suzhou, Jiangsu Province, 215028, China.
Yangyang HuDepartment of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, 430030, China.
Xiaoning GeDepartment of Cardiology, Suzhou Kowloon Hospital, Shanghai Jiaotong University School of Medicine, Suzhou, Jiangsu Province, 215028, China. 18962150582@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMitochondrial oxidative stress (ROS) is a crucial factor in the pathogenesis of dilated cardiomyopathy (DCM). Despite its significance, robust biomarkers for assessing its role remain scarce. This study investigates ROS mechanisms in DCM and identifies associated biomarkers, offering fresh insights into diagnosis and treatment.

methodsWe sourced transcriptomic data from the GEO database and mitochondrial oxidative stress-related genes from GeneCards. Using consensus clustering, we identified 64 genes associated with mitochondrial oxidative stress in DCM and further isolated five hub genes through protein-protein interaction and machine learning techniques. These genes were analyzed for functions related to immunity, drug sensitivity, and single-cell localization. Concurrently, we collected blood samples from DCM patients to validate the hub genes' expression.

resultsThe study identified five hub genes related to mitochondrial oxidative stress: VCL, ABCB1, JAK2, KDR, and NGF. Expression analysis revealed high levels of VCL, ABCB1, KDR, and NGF in the non-failing (NF) group, while JAK2 was elevated in the DCM group (p < 0.05). Diagnostic efficacy, measured by area under the curve (AUC), was significant for VCL (76.4), ABCB1 (80.1), JAK2 (68.2), KDR (78.1), and NGF (71.8). Moreover, several drugs were identified as potential regulators of these hub genes, including Topotecan, CDK9_5576, Acetalax, Afatinib, and GSK591. Notably, VCL showed increased expression in DCM patient blood samples, consistent with transcriptomic and single-cell findings.

conclusionThis research highlights key genes associated with mitochondrial oxidative stress-VCL, ABCB1, JAK2, KDR, NGF-that show differential expression in DCM and myocardial infarction. These findings underscore their diagnostic potential and pave the way for new therapeutic strategies.

Indexed as

Cardiomyopathy, DilatedMitochondriaOxidative StressBiomarkersGene Expression ProfilingHumansJanus Kinase 2Precision MedicineProtein Interaction MapsTranscriptomeBiomarkersJanus Kinase 2BioinformaticsDiagnosisDilated cardiomyopathyImmune infiltrationMitochondriaOxidative stress

Identifiers

PMID40217309
PMCPMC11987231

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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.