Reactive Oxygen species (ROS) homeostasis is essential for normal cell function. Physiological concentrations of ROS control essential cellular processes such as immune response, cell migration, chemotaxis, organelle movement, ion transporter function, cell cycle, and vesicular transport (e.g., endo- and exocytosis). Most importantly, excessive ROS is associated with lipid peroxidation, RNA and DNA damage, and protein oxidation during pathological conditions, leading to cell death, tissue damage and aging.
Many of the cellular functions mentioned above are regulated by cytoskeletal remodeling. ROS can directly modulate cytoskeleton dynamics by modifying the cytoskeleton (actin, tubulin, and intermediate filaments) and cytoskeleton-associated proteins (e.g., GTPases). Additionally, ROS may also participate in signaling pathways governing cytoskeletal remodeling by regulating kinase and phosphatase activity.
This research topic aims to gather recent and novel research on ROS-dependent cytoskeletal signaling during physiological or pathological conditions.
We welcome Original Research Articles, Reviews, Mini Reviews, Methods, Perspectives and Opinion articles. Subtopics include, but are not limited to:
• New mechanisms regulating the crosstalk between ROS and cytoskeleton dynamics in the context of physiological or pathological conditions.
• Oxidative stress inducing changes in organelle localization and function.
• ROS-induced oxidation of cytoskeletal components that modulate cell function.
• Functional and integrative proteomics that identify cytoskeletal changes driven by oxidative stress.
• State-of-the-art techniques to manipulate ROS/cytoskeleton dynamics as putative therapeutic strategies.
Reactive Oxygen species (ROS) homeostasis is essential for normal cell function. Physiological concentrations of ROS control essential cellular processes such as immune response, cell migration, chemotaxis, organelle movement, ion transporter function, cell cycle, and vesicular transport (e.g., endo- and exocytosis). Most importantly, excessive ROS is associated with lipid peroxidation, RNA and DNA damage, and protein oxidation during pathological conditions, leading to cell death, tissue damage and aging.
Many of the cellular functions mentioned above are regulated by cytoskeletal remodeling. ROS can directly modulate cytoskeleton dynamics by modifying the cytoskeleton (actin, tubulin, and intermediate filaments) and cytoskeleton-associated proteins (e.g., GTPases). Additionally, ROS may also participate in signaling pathways governing cytoskeletal remodeling by regulating kinase and phosphatase activity.
This research topic aims to gather recent and novel research on ROS-dependent cytoskeletal signaling during physiological or pathological conditions.
We welcome Original Research Articles, Reviews, Mini Reviews, Methods, Perspectives and Opinion articles. Subtopics include, but are not limited to:
• New mechanisms regulating the crosstalk between ROS and cytoskeleton dynamics in the context of physiological or pathological conditions.
• Oxidative stress inducing changes in organelle localization and function.
• ROS-induced oxidation of cytoskeletal components that modulate cell function.
• Functional and integrative proteomics that identify cytoskeletal changes driven by oxidative stress.
• State-of-the-art techniques to manipulate ROS/cytoskeleton dynamics as putative therapeutic strategies.