Signal transduction by reactive oxygen species

By Toren Finkel. Journal of Cell Biology, 2011

2,204 citations recorded by the source corpus.

Although historically viewed as purely harmful, recent evidence suggests that reactive oxygen species (ROS) function as important physiological regulators of intracellular signaling pathways. The specific effects of ROS are modulated in large part through the covalent modification of specific cysteine residues found within redox-sensitive target proteins. Oxidation of these specific and reactive cysteine residues in turn can lead to the reversible modification of enzymatic activity. Emerging evidence suggests that ROS regulate diverse physiological parameters ranging from the response to growth factor stimulation to the generation of the inflammatory response, and that dysregulated ROS signaling may contribute to a host of human diseases.

Subfields: Immunology, Molecular Biology, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/7ea8eab55680e2e35b938ecde10a51ad5e18be83

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

In Molecular Biology

In Nutrition and Dietetics

Citations in the corpus

The Impact of Oxidative Stress and Inflammation on RPE Degeneration in Non-neovascular AMD (2017, background): “…can act as an important regulator in both physiological and pathological processes, and can be generated from several sources, as reviewed in (Finkel, 2011), including NADPH-dependent oxidases, mitochondrial electron transport chain (ETC) complexes, and other cellular enzymes including…”
Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022, background): “At low to moderate levels, ROS plays an important role in normal cellular processes, serving as secondary messengers in intracellular signalling cascades that mediate cell growth, autophagy, inflammatory and immune function, and contribute to overall redox regulation [16,17].”
T cell lipid peroxidation induces ferroptosis and prevents immunity to infection (2015, background): “Indeed, oxidative stress has been implicated in aging (Lambert et al., 2007) and development of a variety of diseases, including cancer (Toyokuni et al., 1995), type 2 diabetes (Brownlee, 2001), atherosclerosis (Galkina and Ley, 2009), and neurodegeneration (Lin and Beal, 2006).”
NRF2 and the Hallmarks of Cancer. (2018, background): “ROS initiate the apoptotic cascade by oxidation of ASK and activation of p38MAPK and JNK (Finkel, 2011).”
Links between metabolism and cancer. (2012, background): “It is also notable that ROS plays a role in intracellular signaling through alterations of the oxidative status of regulatory protein sulfhydryl moieties (Finkel 2011).”
Mechanisms of activation of the transcription factor Nrf2 by redox stressors, nutrient cues, and energy status and the pathways through which it attenuates degenerative disease (2015, positive): “Evidence from using nonreducing SDS–polyacrylamide gel electrophoresis suggests that the Cys-226 and Cys-613 residues in Keap1 also sense ROS because upon exposure to H2O2 they can form a transient intramolecular disulfide bridge that is associated with brief stabilization of Nrf2 protein [251].”
Reactive Oxygen Species and Antioxidant Defense in Plants under Abiotic Stress: Revisiting the Crucial Role of a Universal Defense Regulator (2020, background): “Therefore, a steady balance between ROS generation and ROS scavenging systems is strongly synchronized over time and space, working together with the cellular redox-sensitive components to shape and finely adapt downstream signaling procedures in a cell-specific and context-specific approach [66,67]”
Oxidative Stress in Cardiovascular Diseases: Still a Therapeutic Target? (2019, background): “As already noted in the introduction, free radical production occurs continuously in all cells as part of aerobic life and indeed, basal levels of ROS are imperative for certain cellular functions [7].”
Mitochondrial complex III ROS regulate adipocyte differentiation (2011, positive): “while at higher levels ROS cause damage (Finkel, 2011).”
HIF-1 mediates metabolic responses to intratumoral hypoxia and oncogenic mutations. (2013, neutral): “ROS levels vary widely in cancer cells, with high ROS levels often associated with cell proliferation (43), whereas low ROS levels have been associated with resistance to chemotherapy (44) and the stem cell phenotype (45, 46).”