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

Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE

Original Publication: Basel, Switzerland : MDPI, [2000-

DNA Damage* ; Oxidative Stress* ; Hypertension*; Humans ; Practice Guidelines as Topic

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).

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(FNOl, 00098892) Ministry of Health, Czech Republic - conceptual development of research organization; (UHHK, 00179906) Supported by Ministry of Health, Czech Republic - DRO

Keywords: DDR; DNA damage and strand breaks; ESC guidelines; PARP inhibitors; cardiovascular disease; concept on genesis; heart failure; hypertension; oxidative stress; risk factors and therapy; γH2AX

Date Created: 20241217 Date Completed: 20241217 Latest Revision: 20250104

20250114

PMC11640817

10.3390/ijms252312557

39684269