# Salivary Redox Biomarkers as a Non-Invasive Research Framework for Exploring Redox-Related Cardiac Electrical Vulnerability in Sudden Unexplained Cardiac Death: A Mechanistic and Narrative Review

**Authors:** Ahmed Adel Mansour Kamar, Ioannis Mavroudis, Alin Ciobica, Diana Gheban

PMC · DOI: 10.3390/medicina62020394 · 2026-02-18

## TL;DR

This review explores using non-invasive salivary redox biomarkers to study redox-related cardiac electrical instability linked to sudden unexplained cardiac death.

## Contribution

Introduces the concept of a 'Salivary Redoxome' as a non-invasive framework for studying redox mechanisms in cardiac electrophysiology.

## Key findings

- Salivary redox biomarkers may reflect systemic redox homeostasis and early molecular disturbances in cardiac function.
- Key enzymes like SOD, CAT, and GPx, along with MDA and TAC, show theoretical relevance to cardiac electrical vulnerability.
- Current evidence is exploratory, with no direct clinical validation linking salivary markers to sudden cardiac death.

## Abstract

Sudden unexplained cardiac death (SUCD) is unpredictable, causing major emotional, economic, and productivity loss. In young, apparently healthy individuals, it remains one of the most challenging causes of mortality to understand mechanistically, and no validated molecular biomarkers are currently available to support investigation of subclinical cardiac electrical vulnerability. Conventional clinical assessment tools such as electrocardiography, echocardiography, and genetic testing often fail to detect early molecular disturbances that precede electrical or structural cardiac abnormalities. Recent evidence suggests that oxidative stress and redox imbalance play a crucial mechanistic role in cardiac electrical instability, modulating ion channel function, calcium handling, mitochondrial signaling, and intercellular coupling. This literature review explores the emerging role of salivary redox biomarkers as a non-invasive research framework for exploring redox-related mechanisms relevant to cardiac electrophysiology, introducing the concept of a “Salivary Redoxome”—an integrated oxidative–antioxidative profile measurable in saliva that may reflect systemic redox homeostasis in an exploratory context, without implying myocardial specificity. Key antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), together with oxidative damage indices such as malondialdehyde (MDA) and total antioxidant capacity (TAC), are discussed for their theoretical mechanistic relevance, biological plausibility, and current limitations. Methodological considerations, sources of pre-analytical variability, and challenges related to biomarker specificity and validation are also addressed to contextualize the current evidence base. At present, no direct clinical evidence links salivary oxidative stress markers to sudden unexplained cardiac death or to electrophysiological arrhythmic risk, and their proposed relevance is therefore exploratory and hypothesis-generating. This review positions salivary redox profiling as a research approach rather than a clinical screening, predictive, or preventive tool, and outlines a future research agenda aimed at systematic validation in well-designed prospective studies.

## Linked entities

- **Proteins:** Cat (Catalase), GPX2 (glutathione peroxidase 2)
- **Chemicals:** malondialdehyde (PubChem CID 10964)

## Full-text entities

- **Genes:** CAMK2G (calcium/calmodulin dependent protein kinase II gamma) [NCBI Gene 818] {aka CAMK, CAMK-II, CAMKG, MRD59}, CAT (catalase) [NCBI Gene 847], SOD1 (superoxide dismutase 1) [NCBI Gene 6647] {aka ALS, ALS1, HEL-S-44, IPOA, SOD, STAHP}
- **Diseases:** cardiac arrest (MESH:D006323), genetic ion-channelopathies (MESH:D053447), inflammation (MESH:D007249), injury to (MESH:D014947), cardiovascular, metabolic, and neurodegenerative diseases (MESH:D019636), Brugada syndrome (MESH:D053840), sleep disturbances (MESH:D012893), Mitochondrial dysfunction (MESH:D028361), premature ventricular complex burden (MESH:D018879), cardiac electrical instability (MESH:D004556), arrhythmic (OMIM:212500), oral diseases (MESH:D009059), arrhythmia (MESH:D001145), cardiomyopathies (MESH:D009202), SCD (MESH:D016757), infections (MESH:D007239), catecholaminergic polymorphic ventricular tachycardia (MESH:C536334), cardiovascular disease (MESH:D002318), Sudden death (MESH:D003645), acute myocardial infarction (MESH:D009203), ischemic heart disease (MESH:D017202), cardiac deaths (MESH:D003643), sudden "unexpected" death (MESH:D000080485), viral infection (MESH:D014777), ventricular fibrillation (MESH:D014693), cardiac abnormalities (MESH:D018376), periodontal disease (MESH:D010510), long QT syndrome (MESH:D008133), ventricular tachycardia (MESH:D017180), arrhythmogenic (MESH:D019571), HF (MESH:D006333), QT dispersion (MESH:C563184), hypertrophic (MESH:D002312), myocardial pathology (MESH:D005598), cardiac (MESH:D006331), CAD (MESH:D003324)
- **Chemicals:** uric acid (MESH:D014527), ascorbic acid (MESH:D001205), MDA (MESH:D008315), superoxide (MESH:D013481), Ca2+ (-), hydrogen peroxide (MESH:D006861), K+ (MESH:D011188), Na+ (MESH:D012964), calcium (MESH:D002118), ROS (MESH:D017382), ATP (MESH:D000255), glutathione (MESH:D005978), lipid (MESH:D008055)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12942136/full.md

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Source: https://tomesphere.com/paper/PMC12942136