ATAD2 has received extensive attention in recent years as one prospective oncogene with tumor-promoting features in many malignancies. ATAD2 is a highly conserved bromodomain family protein that exerts its biological functions by mainly AAA ATPase and bromodomain. ATAD2 acts as an epigenetic decoder and transcription factor or co-activator, which is engaged in cellular activities, such as transcriptional regulation, DNA replication, and protein modification. ATAD2 has been reported to be highly expressed in a variety of human malignancies, including gastrointestinal malignancies, reproductive malignancies, urological malignancies, lung cancer, and other types of malignancies. ATAD2 is involved in the activation of multiple oncogenic signaling pathways and is closely associated with tumorigenesis, progression, chemoresistance, and poor prognosis, but the oncogenic mechanisms vary in different cancer types. Moreover, the direct targeting of ATAD2’s bromodomain may be a very challenging task. In this review, we summarized the role of ATAD2 in various types of malignancies and pointed out the pharmacological direction.

Postoperative cognitive dysfunction (POCD) is a common complication in older surgical patients. While its pathogenesis remains unclear, ferroptosis—an iron-dependent form of cell death driven by lipid peroxidation—has emerged as a key mechanism in neurodegeneration. This review proposes that aging creates a ferroptosis-prone environment in the brain through iron dyshomeostasis, impaired antioxidant defenses, and enrichment of polyunsaturated fatty acids, and that surgical trauma and anesthetic exposure may trigger ferroptosis by activating interconnected pathways such as neuroinflammation, blood-brain barrier disruption, and oxidative stress, leading to neuronal injury in cognition-critical regions like the hippocampus. However, the available evidence is largely correlative, and whether ferroptosis acts as a proximal driver of neuronal death or as a late consequence of pre-existing damage remains undetermined. We dissect the core molecular machinery (GPX4, ACSL4, NCOA4, Nrf2) and emerging regulators (MD2/Hepcidin, CPT1A, RUNX1/RBM47/cGAS-STING, miRNAs, mitophagy, gut microbiota-exosome axis). Therapeutic strategies including iron chelators, lipophilic antioxidants, natural products, physical therapies, and nanomaterials are reviewed, but most remain preclinical. Elucidating the role of ferroptosis may open new avenues for early diagnosis, targeted prevention, and effective treatment, provided that causality can be rigorously established.