Redox Imbalance in Inflammation: The Interplay of Oxidative and Reductive Stress DOI Creative Commons
Francesco Bellanti, Anna Rita Daniela Coda, Maria Incoronata Trecca

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(6), P. 656 - 656

Published: May 29, 2025

Redox imbalance plays a pivotal role in the regulation of inflammation, influencing both onset and progression various inflammatory conditions. While pro-inflammatory oxidative stress (OS) is well established, impact reductive (RS)—a condition marked by excessive reducing equivalents such as NADH, NADPH, reduced glutathione (GSH)—remains underappreciated. This review offers novel integrative perspective analyzing how OS RS act not merely opposition, but interconnected modulators immune function. We explore mechanisms through which activates pathways, RS, when sustained, can paradoxically impair defense, alter redox-sensitive signaling, contribute to disease progression. Emphasis placed on dynamic interplay between these redox extremes their combined contribution pathogenesis chronic diseases, including autoimmune, cardiovascular, neuroinflammatory disorders. Additionally, we evaluate therapeutic strategies that target homeostasis, arguing for shift from antioxidant-centric treatments approaches consider bidirectional nature dysregulation. framework may inform development more precise interventions inflammation-related diseases.

Language: Английский

In Silico Targeting and Immunological Profiling of PpiA in Mycobacterium tuberculosis: A Computational Approach DOI Creative Commons
Mohammad Javad Nasiri,

Lily Rogowski,

Vishwanath Venketaraman

et al.

Pathogens, Journal Year: 2025, Volume and Issue: 14(4), P. 370 - 370

Published: April 9, 2025

Tuberculosis (TB) remains a leading cause of mortality, with drug resistance highlighting the need for new vaccine targets. Peptidyl-prolyl isomerase A (PpiA), conserved Mycobacterium tuberculosis (Mtb) protein, plays role in bacterial stress adaptation and immune evasion, making it potential target immunotherapy. This study uses computational methods to assess PpiA's antigenicity, structural integrity, immunogenic potential. The PpiA sequence was retrieved from NCBI analyzed antigenicity allergenicity using VaxiJen, AllerTOP, AllergenFP. Physicochemical properties were evaluated ProtParam, models generated through PSIPRED SWISS-MODEL. Structural validation performed MolProbity, QMEANDisCo, ProSA-Web. B-cell epitopes predicted BepiPred 2.0 IEDB, while T-cell mapped via IEDB's MHC-I MHC-II tools. Epitope conservation across Mtb strains confirmed ConSurf. Results indicate is highly antigenic, non-allergenic, stable, several identified both B- T-cells. supports as promising TB development.

Language: Английский

Citations

0
Redox Imbalance in Inflammation: The Interplay of Oxidative and Reductive Stress DOI Creative Commons
Francesco Bellanti, Anna Rita Daniela Coda, Maria Incoronata Trecca

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(6), P. 656 - 656

Published: May 29, 2025

Redox imbalance plays a pivotal role in the regulation of inflammation, influencing both onset and progression various inflammatory conditions. While pro-inflammatory oxidative stress (OS) is well established, impact reductive (RS)—a condition marked by excessive reducing equivalents such as NADH, NADPH, reduced glutathione (GSH)—remains underappreciated. This review offers novel integrative perspective analyzing how OS RS act not merely opposition, but interconnected modulators immune function. We explore mechanisms through which activates pathways, RS, when sustained, can paradoxically impair defense, alter redox-sensitive signaling, contribute to disease progression. Emphasis placed on dynamic interplay between these redox extremes their combined contribution pathogenesis chronic diseases, including autoimmune, cardiovascular, neuroinflammatory disorders. Additionally, we evaluate therapeutic strategies that target homeostasis, arguing for shift from antioxidant-centric treatments approaches consider bidirectional nature dysregulation. framework may inform development more precise interventions inflammation-related diseases.

Language: Английский

Citations

0