The aging central nervous system (CNS) is often marked by myelin degeneration, yet the underlying mechanisms remain elusive. This study delves into the previously unexplored role of autophagy in maintaining CNS myelin during aging. We generated the transgenic mouse line plpCre ^ERT2 ; atg5 ^f/f , enabling selective deletion of the core autophagic component Atg5 in oligodendrocytes (OLs) following tamoxifen administration in adulthood, while analysis was conducted on aged mice. Our findings reveal that oligodendroglial autophagy inactivation leads to significant alterations in myelin protein levels. Moreover, the ultrastructural analysis revealed pronounced myelin deficits and increased degeneration of axons, accompanied by apoptosis, as confirmed by immunohistochemistry. Behaviorally, aged knockout (cKO) mice exhibited marked deficits in learning and memory tasks, indicative of cognitive impairment. Additionally, we observed increased activation of microglia, suggesting an inflammatory response linked to the absence of autophagic activity in OLs. These results underscore the critical role of autophagy in OLs for the preservation of CNS myelin and axonal integrity during aging. Our study highlights autophagy as a vital mechanism for neural maintenance, offering potential therapeutic avenues for combating age‐related neurodegenerative diseases.

Oxygen delivery and reactive oxygen species regulation are tightly linked in physiology, with red blood cells serving both as oxygen transporters and as a key antioxidant barrier. This dual function has motivated decades of research into hemoglobin (Hb)‐based oxygen carriers (HBOCs), yet conventional designs remain susceptible to oxidative damage and lack the redox machinery of erythrocytes. In parallel, nanozymes—nanomaterials with enzyme‐mimetic catalytic activities—have emerged as powerful tools in redox medicine. Their integration with HBOCs has created a new class of self‐protecting, multifunctional, and stimuli‐responsive oxygen therapeutics. This review summarizes the foundations and biomedical potential of nanozyme‐integrated HBOCs and Hb‐derived nanozymes. We outline how metal, carbon, and metal–organic framework nanozymes replicate key antioxidant functions, including superoxide dismutase‐, catalase‐, and peroxidase‐like activity. Embedding such nanozymes into HBOCs imparts intrinsic oxidative protection and additional capabilities such as carbonic anhydrase‐like catalysis, transforming passive oxygen carriers into intelligent blood substitutes. We then highlight applications beyond transfusion, including wound healing, where photothermal nanozyme–HBOC hybrids enable light‐controlled oxygen release and antibacterial action, and cancer therapy, where catalytic HBOCs alleviate tumor hypoxia and enhance radiotherapy, photothermal therapy, and photodynamic therapy. Finally, we discuss Hb‐derived and erythrocyte‐templated nanozymes for biosensing, radioprotection, and infection control.

Hypertrophic cardiomyopathy (HCM) is a heart muscle disease associated with an increased risk for sudden cardiac death (SCD). Cytokeratin 18-based proteins, such as M30 and M65 antigens, are known cell-death biomarkers. M30 antigen is released from cells during apoptosis, and M65 antigen is released during cell death from any cause, such as apoptosis or necrosis. We aimed to study the expression of M30 and M65 antigens in peripheral blood obtained by 46 HCM patients and compare with 27 age- and sex-matched patients without HCM. We also investigated the CK18 expression in myocardium from postmortem HCM hearts. M30 and M65 antigens were significantly increased in the HCM vs. non-HCM group (Μ30: 338 ± 197 U/uL vs. 206 ± 166 U/uL, p = 0.003; M65: 428 ± 224 U/uL vs. 246 ± 214 U/uL, p = 0.001), and HCM patients with a higher expression of these markers (M30: 417 ± 208 vs. 271 ± 162 U/uL, p = 0.011; M65: 518 ± 242 vs. 351 ± 178 U/uL, p = 0.011) had a higher risk for SCD. In HCM, both apoptosis and necrosis are increased, but particularly necrosis (M30/M65 ratio: 0.75 ± 0.09 vs. 0.85 ± 0.02, p < 0.001). CK18 is expressed in the HCM myocardium (1.767 ± 0.412 vs. 0.537 ± 0.383, % of area, p = 0.0058). Therefore, M30 and M65 antigens may be novel biomarkers in HCM.