Evidence map›Paper›PMID 39684269›Full record

ReviewInternational journal of molecular sciences2024

Oxidative DNA Damage and Arterial Hypertension in Light of Current ESC Guidelines.

Radka Hazuková, Zdeněk Zadák, Miloslav Pleskot, Petr Zdráhal, Martin Pumprla, Miloš Táborský

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

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

  1. Pooled it
  2. Article
  3. Redox Control in Platelet Activity and Therapy.Antioxidants (Basel, Switzerland) · 2025
    Review
  4. Article
  5. Article
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

6 authors.

Radka HazukováDepartment of Internal Medicine I-Cardiology, University Hospital Olomouc and Faculty of Medicine and Dentistry, Palacky University Olomouc, 77900 Olomouc, Czech Republic.
Zdeněk ZadákIIIrd Department of Internal Medicine-Gerontology and Metabolism, Medical Faculty in Hradec Králové, University Hospital Hradec Králové, Charles University Prague, 50003 Hradec Králové, Czech Republic.ORCID 0000-0002-7391-8619
Miloslav PleskotDepartment of Cardiology and Internal Medicine, Profi-Kardio, s.r.o., 50801 Hořice, Czech Republic.
Petr ZdráhalDepartment of Internal Medicine I-Cardiology, University Hospital Olomouc and Faculty of Medicine and Dentistry, Palacky University Olomouc, 77900 Olomouc, Czech Republic.
Martin PumprlaDepartment of Internal Medicine I-Cardiology, University Hospital Olomouc and Faculty of Medicine and Dentistry, Palacky University Olomouc, 77900 Olomouc, Czech Republic.ORCID 0009-0002-2277-5416
Miloš TáborskýDepartment of Internal Medicine I-Cardiology, University Hospital Olomouc and Faculty of Medicine and Dentistry, Palacky University Olomouc, 77900 Olomouc, Czech Republic.ORCID 0000-0002-5036-2347

Funding

Ministry of Health, Czech Republic - conceptual development of research organization (FNOl, 00098892)Supported by Ministry of Health, Czech Republic - DRO (UHHK, 00179906)
6 · The paper itself

Abstract

A new insight into oxidative stress is based on oxidative deoxyribonucleic acid (DNA) damage. DNA is the pivotal biopolymer for life and health. Arterial hypertension (HT) is a globally common disease and a major risk factor for numerous cardiovascular (CV) conditions and non-cardiac complications, making it a significant health and socio-economic problem. The aetiology of HT is multifactorial. Oxidative stress is the main driver. Oxidative DNA damage (oxidised guanosine (8OHdG), strand breaks (SSBs, DSBs)) seems to be the crucial and initiating causal molecular mechanism leading to HT, acting through oxidative stress and the resulting consequences (inflammation, fibrosis, vascular remodelling, stiffness, thickness, and endothelial dysfunction). In light of the current European Society of Cardiology (ESC) guidelines with defined gaps in the evidence, this manuscript, for the first time, (1) summarizes evidence for oxidative DNA damage in HT and other CV risk factors, (2) incorporates them into the context of known mechanisms in HT genesis, (3) proposes the existing concept of HT genesis innovatively supplemented with oxidative DNA damage, and (4) mentions consequences such as promising new targets for the treatment of HT (DNA damage response (DDR) pathways).

Indexed as

DNA DamageHypertensionOxidative StressHumansPractice Guidelines as Topiccardiovascular diseaseconcept on genesisDDRDNA damage and strand breaksESC guidelinesheart failurehypertensionoxidative stressPARP inhibitorsrisk factors and therapyγH2AX

Identifiers

PMID39684269
PMCPMC11640817

What Socratic holds

Textmetadata
LicenceCC BY
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.