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The dysregulated accumulation of reactive oxygen species (ROS) and reactive nitrogen species disrupts redox homeostasis, triggering oxidative stress (OS) and driving pathophysiological changes across multiple organ systems. OS modulates critical signaling pathways, induces inflammation, impairs mitochondrial function, alters metabolic homeostasis, and dysregulates autophagy, contributing to disease progression. While prior research has largely focused on OS within single-organ diseases (e.g., neurodegenerative, cardiovascular, and oncological disorders), the systemic role of OS in pan-organ diseases and interorgan communication remains insufficiently explored. This review integrates multidisciplinary evidence to elucidate the biological functions of OS in cellular signaling, homeostasis, and cross-organ crosstalk. It systematically dissects OS-driven molecular mechanisms and pathophysiological networks across 10 major organ systems, including the nervous, cardiovascular, oncological, hepatic, and renal systems. Furthermore, it critically examines OS-related therapeutic targets, including antioxidant and ROS-generating enzymes, and explores synergistic redox-based therapeutic strategies. By moving beyond traditional single-organ paradigms, this review constructs a holistic framework to decode the systemic impact of OS, offering novel insights into disease mechanisms and therapeutic innovations. Ultimately, it lays the foundation for precision medicine approaches aimed at mitigating OS-driven diseases and improving multiorgan health outcomes.
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http://dx.doi.org/10.1002/mco2.70268 | DOI Listing |
Biochim Biophys Acta Biomembr
September 2025
Instituto de Física, Universidade Federal de Goiás, Goiânia, GO, Brazil. Electronic address:
Three antileishmanial compounds incorporating a butylated hydroxytoluene (BHT) moiety and an acrylate-based Michael acceptor scaffold were rationally designed from the lead structures LQFM064 and LQFM332, which feature a chalcone-derived core. Their activities against Leishmania (L.) amazonensis were evaluated.
View Article and Find Full Text PDFChem Biodivers
September 2025
School of Pharmaceutical Science, Yunnan Key Laboratory of Pharmacology for Natural Products/College of Modern Biomedical Industry, NHC Key Laboratory of Drug Addiction Medicine, Kunming Medical University, Kunming, P. R. China.
20(R)-ginsenoside Rg3 can reduce the effects of oxidative stress and cell death in cerebral ischemia‒reperfusion injury (CIRI). Neuroinflammation is crucial post-CIRI, but how 20(R)-Rg3 affects ischemia‒reperfusion-induced neuroinflammation is unclear. To study 20(R)-Rg3's effects on neuroinflammation and neuronal preservation in stroke models and explore toll-like receptor 4/myeloid differentiation factor-88/nuclear factor kappa B (TLR4/MyD88/NF-κB) pathway mechanisms.
View Article and Find Full Text PDFJ Agric Food Chem
September 2025
Department of Food Science and Engineering, Ningbo University, Ningbo 315211, P.R. China.
Sleep deprivation (SD) is a major contributor to cognitive impairment, often accompanied by central neuroinflammation and gut microbiota dysbiosis. The tryptophan (TRP) pathway, activated via indoleamine 2,3-dioxygenase (IDO), serves as a critical link between immune activation and neuronal damage. Umbelliferone (UMB), a naturally occurring coumarin compound, possesses anti-inflammatory, antioxidant, and microbiota-modulating properties.
View Article and Find Full Text PDFElife
September 2025
Department of Biology, University of Copenhagen, Copenhagen, Denmark.
Sickness-induced sleep is a behavior conserved across species that promotes recovery from illness, yet the underlying mechanisms are poorly understood. Here, we show that interleukin-6-like cytokine signaling from the gut to brain glial cells regulates sleep. Under healthy conditions, this pathway promotes wakefulness.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Emergency, The People's Hospital of Guangxi Zhuang Autonomous Region and Research Center of Medical Sciences, Guangxi Academy of Medical Sciences, Nanning, Guangxi, China.
Radiotherapy, a prevalent and effective treatment for various malignancies, often causes collateral damage to normal skin and soft tissues in the irradiated area. To address this, we developed a novel approach combining SVFG-modified adipose-derived high-activity matrix cell clusters (HAMCC) with concentrated growth factors (CGF) to enhance regeneration and repair of radiation-induced skin and soft tissue injuries. Our study included cellular assays, wound healing evaluations, and histological analyses.
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