Novel Oxidative Stress Biomarkers with Risk Prognosis Values in Heart Failure

Ng, Mei Li; Ao, Xu; Yap, Kwan Yi; Ng, Jun Jie; Goh, Eugene Chen Howe; Khoo, Benjamin Bing Jie; Richards, A. Mark; Drum, Chester Lee

doi:10.3390/biomedicines11030917

Cited by 22 publications

(22 citation statements)

References 215 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…DUOX, as a member of NADPH oxidase family, participated directly in generating hydrogen peroxide/ROS [ 29 ]. In normal condition, there is a balance between ROS and antioxidants, but the excessive amounts of ROS would result in various CVDs, including heart failure [ 4 ]. In this study, we found the increased DUOX1 expression levels in DOX-induced cellular heart failure model, suggesting that DUOX1 may contribute to heart failure development.…”

Section: Discussionmentioning

confidence: 99%

“…The underlying mechanism of DUOX1 in regulating heart failure has been also explored. It is well-known that heart failure development is associated with oxidative stress, which might be caused by the complex effects of ROS [ 4 ]. DUOX1-induced ROS production has also been shown in various diseases, such as DUOX1 nasal polyposis, allergy and asthma, chronic obstructive pulmonary disease, lung fibrosis and cancer [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

“…It is reported that oxidative stress was one of the main causes of heart failure development [ 4 ]. Oxidative stress is described as a condition of excess reactive oxygen species (ROS) relative to antioxidant defense and ROS is known to play a prominent role in the pathogenesis of various cardiac disorders, such as myocardial infarction and heart failure [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Upregulated dual oxidase 1-induced oxidative stress and caspase-1-dependent pyroptosis reflect the etiologies of heart failure

Li,

Xia,

Chen

et al. 2024

BMC Mol and Cell Biol

View full text Add to dashboard Cite

Background Oxidative stress is implicated in the pathogenesis of heart failure. Dual oxidase 1 (DUOX1) might be important in heart failure development through its mediating role in oxidative stress. This study was designed to evaluate the potential role of DUOX1 in heart failure. Materials and methods AC16 cells were treated with 2 µmol/L of doxorubicin (DOX) for 12, 24, and 48 h to construct a heart failure model. DUOX1 overexpression and silencing in AC16 cell were established. DUOX1 expression was detected by Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Pyroptosis and reactive oxygen species (ROS) production were measured by flow cytometry. Results Increased DUOX1 expression levels were observed after DOX treatment for 24 h in AC16 cells. DUOX1 silencing inhibited DOX-induced pyroptosis and ROS production. The release of IL-1β, IL-18, and lactate dehydrogenase (LDH), and expression levels of pyroptosis-related proteins were also decreased. DUOX1 overexpression increased pyroptosis, ROS production, IL-1β, IL-18, and LDH release, and pyroptosis-related protein expression. N-acetyl-cysteine (NAC) significantly reversed DUOX1-induced pyroptosis, ROS, and related factors. Conclusion These results suggest that DUOX1-derived genotoxicity could promote heart failure development. In the process, oxidative stress and pyroptosis may be involved in the regulation of DUOX1 in heart failure.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Upregulated dual oxidase 1-induced oxidative stress and caspase-1-dependent pyroptosis reflect the etiologies of heart failure

Li,

Xia,

Chen

et al. 2024

BMC Mol and Cell Biol

View full text Add to dashboard Cite

show abstract

“…163 Nitrotyrosine, a specific peroxynitrite-mediated protein modification, is also considered as a biomarker of protein oxidation. 178,182,183 Positive correlations have been reported between nitrotyrosine and human colorectal carcinoma, 184,185 prostate cancer 186 and gastric cancer. 187 Higher levels of nitrotyrosine were detected in H. pylori-infected gastric cancer patients than those without evidence of bacterium infection.…”

Section: Protein Damagementioning

confidence: 99%

“…Nitrotyrosine, a specific peroxynitrite‐mediated protein modification, is also considered as a biomarker of protein oxidation 178,182,183 . Positive correlations have been reported between nitrotyrosine and human colorectal carcinoma, 184,185 prostate cancer 186 and gastric cancer 187 .…”

Section: Host Damage and Gastric Cancermentioning

confidence: 99%

Reactive oxygen species and gastric carcinogenesis: The complex interaction between Helicobacter pylori and host

Wu,

Chen,

Chen

et al. 2023

Helicobacter

View full text Add to dashboard Cite

Helicobacter pylori (H. pylori) is a highly successful human pathogen that colonizes stomach in around 50% of the global population. The colonization of bacterium induces an inflammatory response and a substantial rise in the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), mostly derived from host neutrophils and gastric epithelial cells, which play a crucial role in combating bacterial infections. However, H. pylori has developed various strategies to quench the deleterious effects of ROS, including the production of antioxidant enzymes, antioxidant proteins as well as blocking the generation of oxidants. The host's inability to eliminate H. pylori infection results in persistent ROS production. Notably, excessive ROS can disrupt the intracellular signal transduction and biological processes of the host, incurring chronic inflammation and cellular damage, such as DNA damage, lipid peroxidation, and protein oxidation. Markedly, the sustained inflammatory response and oxidative stress during H. pylori infection are major risk factor for gastric carcinogenesis. In this context, we summarize the literature on H. pylori infection‐induced ROS production, the strategies used by H. pylori to counteract the host response, and subsequent host damage and gastric carcinogenesis.

show abstract

Clustering Based on Laboratory Data in Patients With Heart Failure Admitted to the Intensive Care Unit

Nemati,

Mohammadi,

Hooshanginezhad

2024

Clinical Laboratory Analysis

View full text Add to dashboard Cite

BackgroundHeart failure (HF) is a common condition that imposes a significant burden on healthcare systems. We aimed to identify subgroups of patients with heart failure admitted to the ICU using routinely measured laboratory biomarkers.MethodsA large dataset (N = 1176) of patients with heart failure admitted to the ICU at the Beth Israel Deaconess Medical Center in Boston, USA, between June 1, 2001, and October 31, 2012, was analyzed. We clustered patients to identify laboratory phenotypes. Cluster profiling was then performed to characterize each cluster, using a binary logistic model.ResultsTwo distinct clusters of patients were identified (N = 679 and 497). There was a significant difference in the mortality rate between Clusters 1 and 2 (50 [7.4%] vs. 109 [21.9%], respectively, p < 0.001). Patients in the Cluster 2 were significantly older (mean [SD] age = 72.35 [14.40] and 76.37 [11.61] years, p < 0.001) with a higher percentage of chronic kidney disease (167 [24.6%] vs. 262 [52.7%], respectively, p < 0.001). The logistic model was significant (Log‐likelihood ratio p < 0.001, pseudo R2 = 0.746) with an area under the curve of 0.905. The odds ratio for leucocyte count, mean corpuscular volume (MCV), red blood cell (RBC) distribution width, hematocrit (HcT), lactic acid, blood urea nitrogen (BUN), serum potassium, magnesium, and sodium were significant (all p < 0.05).ConclusionLaboratory data revealed two phenotypes of ICU‐admitted patients with heart failure. The two phenotypes are of prognostic importance in terms of mortality rate. They can be differentiated using blood cell count, kidney function status, and serum electrolyte concentrations.

show abstract

Novel Oxidative Stress Biomarkers with Risk Prognosis Values in Heart Failure

Cited by 22 publications

References 215 publications

Upregulated dual oxidase 1-induced oxidative stress and caspase-1-dependent pyroptosis reflect the etiologies of heart failure

Upregulated dual oxidase 1-induced oxidative stress and caspase-1-dependent pyroptosis reflect the etiologies of heart failure

Reactive oxygen species and gastric carcinogenesis: The complex interaction between Helicobacter pylori and host

Clustering Based on Laboratory Data in Patients With Heart Failure Admitted to the Intensive Care Unit

Contact Info

Product

Resources

About