ROS and ROS-Mediated Cellular Signaling

Area of Science:

• Cellular Biology
• Biochemistry
• Pathophysiology

Background:

• Increased reactive oxygen species (ROS) are linked to cellular dysfunction.
• ROS signaling pathways are implicated in numerous diseases, including atherosclerosis, diabetes, neurodegeneration, inflammation, and aging.
• Existing literature details ROS impacts on signaling pathways but lacks a systemic summary.

Purpose of the Study:

• To provide a comprehensive review of intracellular ROS generation and homeostasis.
• To elucidate the mechanisms and targets through which ROS influence cellular processes.
• To consolidate understanding of ROS interactions with critical cell-signaling pathways and protein systems.

Main Methods:

• Literature review focusing on ROS generation, homeostasis, and signaling.
• Analysis of ROS interactions with specific cell-signaling proteins (NF-κB, MAPKs, Keap1-Nrf2-ARE, PI3K-Akt).
• Examination of ROS effects on ion channels, transporters, protein kinases, and the Ubiquitination/Proteasome System.

Main Results:

• Detailed overview of intracellular ROS production and balance mechanisms.
• Identification of key ROS targets, including signaling proteins, ion channels (Ca2+), and the mitochondrial permeability transition pore (mPTP).
• Elucidation of ROS-mediated modifications to protein kinase activity and the Ubiquitination/Proteasome System.

Conclusions:

• A systemic understanding of ROS homeostasis and signaling is crucial for comprehending associated pathologies.
• ROS significantly modulate critical cellular functions by targeting diverse signaling proteins and systems.
• This review synthesizes current knowledge, highlighting the complex role of ROS in health and disease.