Cellular macromolecules involved in DNA damage and redox homeostasis

Cellular macromolecules involved in DNA damage and redox homeostasis refer to a broad and heterogeneous group of proteins, nucleic acids, and lipids that collectively maintain genomic integrity and balance reactive oxygen species (ROS) within the cell [Ray et al., 2012, Cell Signal]. This functional category includes critical DNA repair enzymes such as Poly (ADP-ribose) polymerase 1 (PARP1) and Ataxia-telangiectasia mutated (ATM), as well as master redox regulators like Nuclear factor erythroid 2-related factor 2 (NRF2) [Lord & Ashworth, 2012, Nature]. These molecules work in concert to detect chemical or radiation-induced lesions and initiate corrective signaling or antioxidant defenses to prevent mutations and cellular dysfunction [Sies, 2015, Redox Biol]. In many pathological states, such as cancer and neurodegeneration, the equilibrium between DNA damage and redox control is disrupted, leading to genomic instability or chronic oxidative damage [Hoeijmakers, 2009, N Engl J Med]. Therapeutic strategies targeting these systems often involve inhibiting repair mechanisms to induce synthetic lethality in tumors or activating protective pathways to mitigate oxidative stress in chronic diseases [Kansanen et al., 2013, Redox Biol]. Because this term describes a complex biological network rather than a single druggable entity, it is classified as a therapeutic area or category rather than a specific molecular target.

Other names

DNA damage response (DDR) componentsRedox-sensitive macromoleculesAntioxidant and DNA repair systemsGenomic integrity and oxidative stress factors

Modulation of DNA repair efficiency (e.g., PARP inhibition) or induction of antioxidant gene expression via the NRF2/KEAP1 pathway to alter cellular survival under stress.