ROS and ROS-Mediated Cellular Signaling

By Jixiang Zhang, Xiaoli Wang, Vikash Vikash, Qing Ye, Dandan Wu, Yulan Liu, W. Dong. Oxidative Medicine and Cellular Longevity, 2016

1,725 citations recorded by the source corpus.

It has long been recognized that an increase of reactive oxygen species (ROS) can modify the cell-signaling proteins and have functional consequences, which successively mediate pathological processes such as atherosclerosis, diabetes, unchecked growth, neurodegeneration, inflammation, and aging. While numerous articles have demonstrated the impacts of ROS on various signaling pathways and clarify the mechanism of action of cell-signaling proteins, their influence on the level of intracellular ROS, and their complex interactions among multiple ROS associated signaling pathways, the systemic summary is necessary. In this review paper, we particularly focus on the pattern of the generation and homeostasis of intracellular ROS, the mechanisms and targets of ROS impacting on cell-signaling proteins (NF-κB, MAPKs, Keap1-Nrf2-ARE, and PI3K-Akt), ion channels and transporters (Ca2+ and mPTP), and modifying protein kinase and Ubiquitination/Proteasome System.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/d5ce217ed367361102b36e233fb65f790f2246c2

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Citations in the corpus

ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells (2019, background): “Reactive oxygen species (ROS) are formed as natural by-products of normal cell activity and participate in cellular signaling [1].”
Activation of Nrf2/HO-1 signaling: An important molecular mechanism of herbal medicine in the treatment of atherosclerosis via the protection of vascular endothelial cells from oxidative stress (2021, background): “In addition, these inflammatory factors also promote the production of ROS and adhesion molecules in endothelial cells, further exacerbating endothelial injury [45].”
Reactive Oxygen Species Signaling and Oxidative Stress: Transcriptional Regulation and Evolution (2024, background): “…damaging effects, recent research has unveiled the dual role of ROS as vital signaling molecules engaged in regulating numerous biological processes [4]. conserved in various life forms, and it becomes toxic at concentrations above 0.5 × 10 − 4 M, at which it induces cell apoptosis [41].”
Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives (2022, background): “t si l ic l l l, str t s; c , t ct s i e s ste to ro i e efe se a ai st forei o ies [73], a are also se for t e for ation of cell structures such as protein complexes [74].”
ROS and the DNA damage response in cancer (2018, neutral): “g·H2O2 regulating NFκB, MAPK pathways) [11].”
Reactive Oxygen Species: Drivers of Physiological and Pathological Processes (2020, positive): “42,43 Thus, ROS control pro-inflammatory signaling, pro-fibrotic signaling, cell proliferation, apoptosis and a range of other biological processes without triggering a requirement for macromolecular damage.”