Mechanisms and therapeutic strategies of asthma: from bench to bedside.

Post‐stroke cognitive impairment (PSCI) occurs in approximately 60% of patients with stroke in the first year after onset []. There is an emerging consensus that the risk of PSCI is determined by the interplay of various factors, including modifiable and non‐modifiable risk factors, comorbidities, index stroke characteristics, features of acute infarct or hemorrhage, and the overall burden of pre‐existing brain injury []. The most prevalent deficits were observed in learning, verbal and figural episodic memory, constructive abilities, and selective attention, while deficits were identified across all cognitive domains []. Consequently, there is an imperative need for precise diagnosis, prompt intervention, and effective prevention of PSCI. Spectrins are a class of cytoskeletal proteins that are widely expressed in the mammalian nervous system, and pathogenic variants in , , , and , four of the six genes encoding neuronal spectrins, have been associated with neurological disorders []. Among these, has been reported to interact with solute carrier family 7 member 11 (SLC7A11, also termed xCT), facilitating its membrane localization and suppressing ferroptosis in non‐small cell lung cancer []. Ferroptosis, characterized by lipid peroxidation and iron accumulation, has also been implicated in ischemic stroke (IS), and alterations in ferroptosis‐related genes, such as and , have been observed [, ]. This process is primarily triggered by the disruption of the cellular antioxidant system, particularly the system Xc‐glutathione (GSH)‐GPX4 axis []. Slc7a11 plays a critical role in the import of cysteine, an essential precursor for GSH biosynthesis and antioxidant defense []. However, whether ‐mediated membrane localization of Slc7a11 is involved in PSCI remains unknown. has been reported to be regulated by METTL3‐mediated N6‐methyladenosine (mA) modification in colorectal cancer []. mA modification affects the processing, structure, localization, stability, degradation, and translation of RNAs and their functions, such as RNA‐protein and RNA–RNA interactions []. Generally, the regulation and function of mA modification involve three types of proteins: methyltransferases (writers), RNA‐binding proteins (RBPs, readers), and demethylases (erasers) []. The RBP heterogeneous nuclear ribonucleoproteins A2/B1 (hnRNPA2B1) is a member of the hnRNP family that can recognize and bind specific RNA substrates and DNA motifs, which enables the modulation of their transcription, splicing, processing, transport, stability, and translation, and is involved in the development of neurodegenerative diseases []. Although it has recently been reported to be a key mA regulator of IS [], its specific role and mechanism in PSCI remain unknown. Therefore, this study aimed to evaluate the impact of Hnrnpa2b1/Sptbn2 on neuronal ferroptosis‐related damage in PSCI by subjecting mice to permanent middle cerebral artery occlusion (pMCAO) and mouse hippocampal HT‐22 neurons to oxygen–glucose deprivation (OGD).