Not So Crystal Clear: Pulmonary Crystal-Storing Histiocytosis Without Haematological Disease: A Unique Radiological Manifestation and Review of the Literature.

Traumatic brain injury (TBI) is a major cause of death and long-term neurological disability worldwide (; ; ; ). Despite substantial advances in neurosurgical techniques, intensive care management, and neurocritical monitoring, effective pharmacological interventions remain limited (; ; ). The pathological progression of TBI is commonly divided into primary injury and secondary injury. Primary injury occurs immediately after mechanical trauma and is generally considered irreversible (; ; ; ). In contrast, secondary injury evolves over a prolonged period following the initial insult and contributes substantially to progressive neuronal loss and neurological dysfunction. Therefore, therapeutic strategies aimed at limiting secondary injury have become a major focus of current TBI research. Among the pathological processes involved in secondary injury, oxidative stress is widely recognized as a central contributor to disease progression (; ; ; ). Mechanical trauma disrupts cellular homeostasis and induces mitochondrial dysfunction, calcium overload, and excitotoxicity, leading to excessive production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) (; ; ). The accumulation of these reactive species causes lipid peroxidation, protein oxidation, DNA damage, and impairment of blood brain barrier integrity (; ; ). Moreover, oxidative stress interacts closely with neuroinflammation, ferroptosis, and mitochondrial dysfunction, thereby creating a vicious cycle that amplifies tissue damage. Growing evidence suggests that restoring redox homeostasis may represent an effective approach for mitigating neurological deficits following TBI (; ; ). Considerable efforts have been devoted to the development of antioxidant therapies for TBI (; ; ). However, the clinical efficacy of conventional antioxidants has been disappointing because of their poor stability, rapid clearance, insufficient catalytic capacity, and limited accumulation within injured brain tissues (; ; ). Nanozymes, a class of nanomaterials that possess intrinsic enzyme mimicking catalytic activities, have recently emerged as promising candidates for the treatment of oxidative stress related diseases (; ; ; ). Unlike traditional antioxidants that are consumed during redox reactions, nanozymes can continuously catalyze the conversion of reactive species into less harmful products. Depending on their composition and structure, nanozymes may exhibit activities similar to superoxide dismutase, catalase, glutathione peroxidase, or multiple antioxidant enzymes simultaneously (; ; ). Recent advances in nanotechnology have further enabled the rational design of nanozymes with improved catalytic efficiency, enhanced biocompatibility, imaging capability, and increased accumulation within pathological tissues (; ; ).