Background: Dietary habits influenced by lifestyle and cultural factors play a critical role in health by modulating oxidative stress and inflammation. While diets offer significant benefits, they may also pose risks, such as nutrient deficiencies, emphasizing the need for a balanced approach. Exploring Mediterranean and plant-based diet effects on oxidative stress and inflammation biomarkers may help improve health outcomes and disease prevention strategies. Methods: This study analyzed 65 studies following PRISMA guidelines to evaluate the effects of Mediterranean and plant-based diets on biomarkers of oxidative stress and inflammation in healthy individuals. Results: The Mediterranean diet was weakly associated with reductions in oxidative stress markers, including MDA (ROM: 0.80; 95% CI: 0.57–1.13; p = 0.2092) and 8OHdG (ROM: 0.81; 95% CI: 0.59–1.11; p = 0.1847), as well as inflammation markers such as CRP (ROM: 0.72; 95% CI: 0.42–1.23; p = 0.1545) and IL-6 (ROM: 1.23; 95% CI: 0.97–1.55; p = 0.08). The vegetarian diet significantly reduced CRP (ROM: 0.82; 95% CI: 0.69–0.98; p = 0.0297), while the vegan diet showed a borderline reduction (ROM: 0.81; 95% CI: 0.56–1.17; p = 0.2544), suggesting lower systemic inflammation compared to omnivorous diets. Conclusions: Although all three diets demonstrate potential in reducing oxidative stress and inflammation, the antioxidant effects—especially for the Mediterranean diet—are lower than anticipated, indicating alternative mechanisms. Further research is essential to confirm these findings and clarify the underlying mechanisms to enhance preventive health strategies.

Cigarette smoking is a primary contributor to mortality risks and is associated with various diseases. Among these, COPD represents a significant contributor to global mortality and disability. The objective of this study is to investigate the effect of smoking on a selected battery of variables, with an emphasis on DNA damage. A total of 87 elderly patients diagnosed with COPD, divided into three groups based on their smoking history (current, former, never-smokers), were evaluated using a cross-sectional approach. Clinical features including mortality and inflammatory/oxidative parameters (Lymphocytes/Monocytes, Neutrophils/Lymphocytes, Platelets/Lymphocytes ratio), SII, MDA, 8-Oxo-dG, and IL6 (ELISA assay), as well as DNA damage (comet assay), were investigated. Virus infection, i.e., influenza A virus subtype H1N1, JC polyomavirus (JCPyV), BK polyomavirus (BKPyV), and Torquetenovirus (TTV), was also tested. Current smokers exhibit higher levels of comorbidity (CIRS; p < 0.001), Platelets/Lymphocytes ratio (p < 0.001), systemic immune inflammation (p < 0.05), and DNA damage (p < 0.001). Former smokers also showed higher values for parameters associated with oxidative damage and showed a much lower probability of surviving over 5 years compared to never- and current smokers (p < 0.0017). This study showed a clear interaction between events which are relevant to the oxidative pathway and cigarette smoking. A category of particular interest is represented by former smokers, especially for lower survival, possibly due to the presence of more health problems. Our findings raise also the attention to other parameters which are significantly affected by smoking and are useful to monitor COPD patients starting a program of pulmonary rehabilitation (DNA damage, inflammation parameters, and selected viral infections).

Torque Teno Virus (TTV), an "orphan" virus with unclear pathology, has been associated with various diseases and immune dysfunctions. This study investigates the link between TTV viremia and clinical markers in patients with severe to very severe COPD undergoing respiratory rehabilitation. We analyzed 102 elderly COPD patients, stratified by TTV viremia levels (< or ≥ 4 log10 copies/mL). Clinical markers-including mortality, inflammatory-oxidative parameters (Lymphocyte/Monocyte, Neutrophil/Lymphocyte, and Platelet/Lymphocyte ratios), IL-6 (measured via ELISA assay), and DNA damage (assessed via comet assay)-were evaluated. Of the patients, 62.75 % had TTV viremia levels > 4 log₁₀ copies/mL. No associations were found between TTV levels and sex or obesity. However, higher TTV viremia correlated with increased DNA damage and significantly lower 5-year survival probability. Patients with TTV levels ≥ 4 log₁₀ copies/mL exhibited the lowest survival probability, though DNA damage emerged as a stronger determinant of outcomes. This study raises key scientific questions on the role of TTV in COPD. Specifically, it explores whether TTV may serve as a potential marker for poor prognosis in COPD and whether rehabilitation strategies for these patients could be customized based on DNA damage and/or viremia.

Heart failure (HF) is a syndrome characterized by signs and symptoms resulting from structural or functional cardiac abnormalities, confirmed by elevated natriuretic peptides or evidence of congestion. HF patients are classified according to left ventricular ejection fraction (LVEF). Worsening HF (WHF) is associated with increased short- and long-term mortality, re-hospitalization, and healthcare costs. The standard treatment of HF includes angiotensin-converting enzyme inhibitors, angiotensin receptor–neprilysin inhibitors, mineralocorticoid-receptor antagonists, beta-blockers, and sodium-glucose-co-transporter 2 inhibitors. To manage systolic HF by reducing mortality and hospitalizations in patients experiencing WHF, treatment with vericiguat, a direct stimulator of soluble guanylate cyclase (sGC), is indicated. This drug acts by stimulating sGC enzymes, part of the nitric oxide (NO)–sGC–cyclic guanosine monophosphate (cGMP) signaling pathway, regulating the cardiovascular system by catalyzing cGMP synthesis in response to NO. cGMP acts as a second messenger, triggering various cellular effects. Deficiencies in cGMP production, often due to low NO availability, are implicated in cardiovascular diseases. Vericiguat stimulates sGC directly, bypassing the need for a functional NO-sGC-cGMP axis, thus preventing myocardial and vascular dysfunction associated with decreased sGC activity in heart failure. Approved by the FDA in 2021, vericiguat administration should be considered, in addition to the four pillars of reduced EF (HFrEF) therapy, in symptomatic patients with LVEF < 45% following a worsening event. Cardiac rehabilitation represents an ideal setting where there is more time to implement therapy with vericiguat and incorporate a greater number of medications for the management of these patients. This review covers vericiguat’s metabolism, molecular mechanisms, and drug–drug interactions.

Background: Oxidative stress is a key driver of heart failure (HF) pathophysiology, promoting myocardial injury, inflammation, and remodeling. Although numerous biomarkers of oxidative stress and DNA damage have been investigated in HF, their clinical relevance remains uncertain. This systematic review and meta-analysis aimed to evaluate alterations in these biomarkers in HF patients compared to healthy controls. Methods: A comprehensive search of PubMed, MEDLINE, the Cochrane Library, and Web of Science was conducted in accordance with PRISMA guidelines. Studies reporting oxidative stress or DNA damage biomarkers in HF patients versus controls were included. Random-effects models were used to calculate ratios of means (ROM) with 95% confidence intervals (CI). Heterogeneity and publication bias were assessed using the I² statistic and Begg’s test. Results: Data from 3015 HF patients and 2704 controls were analyzed. HF patients had significantly higher levels of 8-hydroxy-2′-deoxyguanosine (8-OHdG) (ROM = 2.24, 95% CI: 1.75–2.88), malondialdehyde (MDA) (ROM = 1.87, 95% CI: 1.49–2.36) and isoprostanes (ROM = 2.83, 95% CI: 1.97–4.05). Telomere length was significantly shorter (ROM = 0.66, 95% CI: 0.53–0.81), indicating accelerated cellular aging. Considerable heterogeneity was observed across studies. Conclusion: This meta-analysis supports a robust association between oxidative stress, DNA damage, and HF, highlighting the potential role of these biomarkers in disease monitoring and prognosis.

Background: Oxidative stress is a key driver of heart failure (HF) pathophysi-ology, promoting myocardial injury, inflammation, and remodeling. Alt-hough numerous biomarkers of oxidative stress and DNA damage have been investigated in HF, their clinical relevance remains uncertain. This systematic review and meta-analysis aimed to evaluate alterations in these biomarkers in HF patients compared to healthy controls. Methods: A comprehensive search of PubMed, MEDLINE, the Cochrane Li-brary, and Web of Science was conducted in accordance with PRISMA guide-lines. Studies reporting oxidative stress or DNA damage biomarkers in HF pa-tients versus controls were included. Random-effects models were used to calculate ratios of means (ROM) with 95% confidence intervals (CI). Hetero-geneity and publication bias were assessed using the I² statistic and Egger’s test. Results: Data from 2,188 HF patients and 1,073 controls were analyzed. HF patients had significantly higher levels of isoprostanes (ROM = 2.83, 95% CI: 1.97–4.05), 8-hydroxy-2′-deoxyguanosine (8-OHdG) (ROM = 2.24, 95% CI: 1.75–2.88), and malondialdehyde (MDA) (ROM = 1.87, 95% CI: 1.49–2.36). Te-lomere length was significantly shorter (ROM = 0.66, 95% CI: 0.53–0.81), indi-cating accelerated cellular aging. Considerable heterogeneity was observed across studies. Conclusion: This meta-analysis supports a robust association between oxida-tive stress, DNA damage, and HF, highlighting the potential role of these bi-omarkers in disease monitoring and prognosis.