Background Patient-reported outcomes (PROs) are essential for assessing symptomatic adverse events (AEs) from a patient perspective, which significantly impact the quality of life and clinical outcomes in patients with glioma. However, no validated patient-reported outcome measures (PROMs) exist to quantify symptomatic AEs in adult-type diffuse gliomas. Methods The study was conducted in two parts. First, we developed a customised Patient-Reported Outcomes version of the Common Terminology Criteria for Adverse Events (PRO-CTCAE) scale for adult-type diffuse gliomas using the Simplified Chinese PRO-CTCAE® item library, informed by initial item screening, patient pilot testing, and a two-round Delphi survey. Delphi experts were recruited through the National Glioma Multidisciplinary Team (MDT) Alliance (NGMA) and invited by email in June 2022 (1st round) and August 2022 (2nd round). We subsequently conducted a multicentre, prospective, observational cohort study (VERONICA) at 13 glioma treatment centres in China between September 2022 and March 2025. Eligible participants were adults aged 18 years or older with a diagnosis of adult-type diffuse glioma, who were able to understand and complete the questionnaires; patients with severe cognitive impairment, severe language dysfunction, or other conditions precluding questionnaire completion were excluded. The primary outcome was the psychometric performance of the customised PRO-CTCAE scale, including test-retest reliability, convergent validity, known-groups validity, and responsiveness, evaluated longitudinally across repeated study visits. VERONICA is registered with ClinicalTrials.gov, NCT05486923. Findings For the Delphi survey, all seven invited experts from six centres participated in 1st round (response rate 100·0%), with moderate agreement in symptom rankings (Kendall's W = 0·415; p < 0·001). In 2nd round, 16 of 20 invited experts from 14 centres participated (response rate 80·0%), with consistent agreement in expert ratings (Kendall's W = 0·351; p < 0·001). The final version of the customised PRO-CTCAE scale comprised 53 items covering 31 symptoms, together with one open-ended free-text item. For VERONICA, 450 participants were enrolled across 13 glioma treatment centres. Mean age was 49·1 years (SD 12·8), and the mean Karnofsky Performance Status (KPS) at baseline (Visit 2) was 72·2 (SD 17·1). 424 provided data eligible for at least one prespecified psychometric analysis. Test-retest reliability was acceptable (intraclass correlation coefficient [ICC] ≥0·70 for 47 of 53 items). Convergent validity was supported by correlations in the expected direction with matched European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire-Core 30 (EORTC QLQ-C30) domains, with predominantly moderate-to-strong associations (25 items with r ≥ 0·50). Known-groups validity was supported by discrimination between KPS <70 and ≥70 (Cohen's d ≥ 0·20 for 49 of 53 items; p < 0·05 for 43 of 49 items). In Global Impression of Change (GIC)-anchored responsiveness analyses, 37 items showed standardised response means (SRMs) ≥0·20 among participants reporting worsened overall status. Interpretation The customised PRO-CTCAE scale showed robust psychometric performance for adult-type diffuse gliomas. Remote, longitudinal administration supports low-burden quantification of patient-reported symptomatic AEs in clinical trials and routine neuro-oncology practice. Future work should assess implementation in routine care and clinical trials, and extend translation, cultural adaptation, and validation across different languages. Funding Beijing Medical Award Foundation; Shanghai Municipal Health Commission; Department of Science and Technology of Ningxia Hui Autonomous Region; Huashan Hospital, Fudan University (Clinical Research Project).

Background and Purpose: Subarachnoid hemorrhage (SAH) triggers a complex immune response that critically influences early brain injury (EBI) and long-term outcomes. However, the precise spatiotemporal dynamics and heterogeneity of immune cell infiltration and microglial reprogramming remain poorly understood. We aimed to construct a high-resolution immune atlas to delineate cell states, lineage trajectories, and spatial niches following SAH. Methods: We integrated single-cell RNA sequencing (scRNA-seq) of CD45+ immune cells with spatial transcriptomics (ST) in a murine endovascular perforation SAH model. Immune landscapes were profiled at 24 hours (acute phase) and 72 hours (subacute phase) post-injury, compared with sham controls. Advanced bioinformatics integrated transcriptional signatures with spatial localization to map macrophage, neutrophil, and microglial dynamics. Results: Our atlas reveals a coordinated immune transition from acute inflammation to reparative processing. We identified five macrophage, four neutrophil, and eight microglial subsets with distinct spatiotemporal patterns. Notably, we discovered a SAH-specific inflammatory microglial population (MG\_03; Spp1+/Lpl+) that clusters at the rupture site during the acute phase. This subset is transcriptionally distinct from disease-associated microglia (DAM) in other neurodegenerative conditions. Trajectory analysis suggests MG\_03 acts as a signaling hub for immune recruitment before transitioning toward proliferative and reparative states (MG\_06-08) that disperse into the parenchyma by 72 hours. Conclusions: This study provides the first comprehensive spatiotemporal immune atlas of SAH, highlighting the distinct role of the Spp1+ MG\_03 subpopulation in early injury sensing. These findings offer a roadmap for identifying precise therapeutic windows and targeting specific immune subsets to mitigate EBI. ### Competing Interest Statement The authors have declared no competing interest.

Selective autophagy, a lysosome-dependent degradation pathway targeting specific substrates (e.g., mitochondria, protein aggregates), plays a pivotal role in maintaining neuronal homeostasis. Its dysregulation is intricately linked to neurodegenerative diseases, acute brain injuries, and neuroinflammatory disorders. This review elucidates the crosstalk between selective autophagy and key neuropathophysiological processes, including apoptosis, neuroinflammation, oxidative stress, and blood-brain barrier disruption. We delineate the dual roles of selective autophagy through the framework of the neuroautophagic interactome-a network in which kinases (ULK1, TBK1) and effectors (PINK1/Parkin, SQSTM1/p62) collaboratively interpret ubiquitin codes. This integrated signaling nexus functions as a decisive hub that bidirectionally modulates disease progression. Furthermore, we evaluate emerging therapeutic strategies targeting selective autophagy to mitigate neuronal damage, emphasizing its dual role as both a protector and a contributor to disease progression.

BACKGROUND:Primary sellar atypical teratoid/rhabdoid tumor (AT/RT) is a rare, fast-growing, and aggressive embryonal tumor in adults. Awareness of potential "red flags" of this disease is important but difficult for clinicians during preoperative assessment. METHODS:The clinical and radiological data of 3 adult patients diagnosed with primary sellar AT/RT at our institute were retrospectively analyzed. Additionally, the clinical characteristics of 75 individual cases of primary sellar AT/RT identified from 46 publications were reviewed. RESULTS:Sex, age, sellar compression symptoms, magnetic resonance imaging (MRI) characteristics, and pituitary hormone levels of 3 patients from our institute and 75 cases from the literature were analyzed (n = 78). The cohort consisted of 5 (6.4%) males and 73 (94%) females, ranging in age from 20 to 80 years, with a mean age of 47 years. Fifty-three (68%) patients suffered from headaches, 11 (14%) of whom experienced severe headaches or progressive headaches. Forty-one (53%) patients presented with ophthalmoplegia, manifesting symptoms such as ptosis and diplopia. MRI revealed that 42 (54%) patients had sellar masses invading the cavernous sinus, with 11 (14%) cases showing bilateral cavernous sinus involvement. Pituitary-related hormone abnormality was found in 36 (46%) patients, including 19 (24%) patients with hypopituitarism. CONCLUSIONS:Primary sellar AT/RT is an aggressive yet rare malignancy in adults. Rapidly progressive sellar compression symptoms and aggressive MRI characteristics provide crucial clues for the preoperative presumptive diagnosis of this disease.

Background/Objectives: Immune-inflammatory activation is a central feature of aneurysmal subarachnoid hemorrhage (aSAH), yet the epitranscriptomic mechanisms underlying this response remain insufficiently understood. This study aimed to investigate RNA methylation-associated immune dysregulation in aSAH and to identify potential biomarkers and signaling pathways. Methods: Four Gene Expression Omnibus datasets were analyzed to characterize RNA methylation regulator-related immune alterations in aSAH. Single-sample gene set enrichment analysis (ssGSEA), weighted gene co-expression network analysis (WGCNA), and intersection with ImmPort immune genes were used to identify candidate genes. A total of 159 machine learning combinations were evaluated for model construction and external validation. Two-sample Mendelian randomization, single-cell RNA sequencing (scRNA-seq), and CellChat analyses were further performed. Peripheral blood samples from patients with aSAH (n = 12) and matched healthy controls (n = 12) were used for total m6A quantification and quantitative real-time PCR (qRT-PCR) validation, while Western blotting and immunofluorescence were used to validate the protein expression of LIFR, GP130, IGF2BP2, and RBM15B. Results: Eleven RNA methylation regulators were differentially expressed between aSAH and controls in GSE122897. The WGCNA module most strongly associated with RNA methylation regulator-related scores was enriched in immune response and myeloid activation pathways. Intersection analysis identified 25 candidate immune-inflammatory genes associated with RNA methylation regulator-related transcriptional patterns. Among 159 algorithms, an XGBoost-LASSO pipeline selected oncostatin M (OSM) as the key variable, and the resulting RNA methylation regulator-related immune-derived gene signature (RMRIGS) showed good discrimination between aSAH and controls across training and validation cohorts. Mendelian randomization supported a protective association of genetically predicted OSM expression with subarachnoid hemorrhage risk (IVW OR = 0.66, p = 0.014). Single-cell analysis showed that Osm was predominantly enriched in infiltrating Ccr2+ macrophages, whereas Lifr and Il6st were broadly expressed in activated microglial subpopulations, indicating the presence of an Osm - (Lifr + Il6st) communication axis after SAH. Clinically, total m6A levels were increased in peripheral blood samples from patients with aSAH, and OSM, together with several RNA methylation regulators, was upregulated and associated with m6A-related changes. In experimental models, the protein expression levels of LIFR, GP130, IGF2BP2, and RBM15B were all increased after SAH-related stimulation. Conclusions: RNA methylation programs may be involved in immune dysregulation in aSAH. The OSM-centered RMRIGS was associated with disease status and may provide insight into the interaction between peripheral immune activation and post-SAH neuroinflammation. The potential involvement of the OSM-LIFR/GP130 signaling axis and its association with RNA methylation regulator-related alterations warrant further investigation.

According to animal studies, glymphatic–meningeal lymphatic dysfunction contributes to poor prognosis and the development of chronic hydrocephalus after subarachnoid hemorrhage (SAH). This study aimed to evaluate glymphatic function and meningeal lymphatic drainage signal in patients with SAH. SAH patients and healthy controls (HCs) were enrolled and underwent multimodal MRI. Glymphatic function was assessed using the diffusion tensor imaging analysis along the perivascular space (DTI-ALPS) index, free water in white matter (FW-WM), and white matter perivascular space volume fraction (PVSVF-WM). The signal intensity (SI) of meningeal lymphatic vessels (mLVs) and deep cervical lymph nodes (dcLNs) was also quantified as an imaging surrogate of meningeal lymphatic drainage. Compared with HCs, SAH patients exhibited significant impairment of glymphatic function, characterized by a reduced DTI-ALPS index, increased FW-WM, and increased PVSVF-WM, along with reduced SI of the mLVs and dcLNs. Patients with chronic hydrocephalus showed even more pronounced impairment than those with acute SAH. Importantly, reduced DTI-ALPS index and mLV SI loss were identified as independent predictors of chronic shunt-dependent hydrocephalus. Notably, 53.8

Traumatic brain injury (TBI) is among the most devastating condition and involves primary and secondary injury cascades. The blood-brain barrier (BBB) is a selective, semipermeable membrane that tightly controls the brain’s microenvironment for proper neuronal function. Existing evidence demonstrates that TBI impairs the integrity and function of the BBB, leading to not only acute pathological changes but also long-term neuropathological consequences. Multiple BBB-related signaling molecules (e.g., Tie-2, EphB3, and Cav-1) are involved in the pathophysiological processes post-injury. These can result in microcirculatory insufficiency, neurotoxin accumulation, and cerebral edema after TBI. Together, such events synergistically cause axonal damage, neuronal cell death, and neuroinflammatory responses, which underlie the pathogenesis of TBI. In this review, we aim to summarize the pathophysiological roles of BBB breakdown in TBI, survey underlying mechanisms, and discuss therapeutic potential for this notorious disease by regulating the BBB.

The pathological mechanism of acute ischemic stroke (AIS) is complex, and exploring new diagnostic biomarkers and key molecular pathological targets is crucial for improving patient prognosis. The role of epigenetic regulation, especially DNA methylation, in AIS is receiving increasing attention, but its key target genes and clinical translational value still need to be elucidated. This study included 90 case-control groups and used pyrophosphate sequencing to detect the methylation level of β2-adrenergic receptor (ADRB2) promoter in peripheral blood. Using oxygen glucose deprivation/reperfusion (OGD/R) cell models and middle cerebral artery occlusion (MCAO) mouse models, the effects of ADRB2 expression on JAK2/STAT3 and Nrf2/HO-1 pathways, as well as inflammatory and oxidative stress factors, were evaluated using Western blot, ELISA, and other techniques. Intervention study using curcumin. The ADRB2 promoter region in the peripheral blood of AIS patients showed significant hypermethylation, and its level was significantly negatively correlated with ADRB2 mRNA and protein expression. ROC curve analysis shows that the methylation level of specific CpG sites has extremely high predictive value for AIS diagnosis (AUC ≥ 0.9). Functional experiments have confirmed that DNMT1 mediated methylation of ADRB2 increases after ischemia and hypoxia, and the downregulation of ADRB2 protein directly leads to activation of the JAK2/STAT3 pathway and inhibition of the Nrf2/HO-1 pathway, thereby synergistically exacerbating cerebral ischemic injury. Curcumin reverses the high methylation of ADRB2 by inhibiting DNMT1, upregulates ADRB2 expression, effectively improves neurological deficits, and reduces infarct volume, verifying the therapeutic feasibility of targeting this molecular pathological target. This study systematically elucidates for the first time that high methylation of ADRB2 promoter is a new biomarker and key pathological mechanism node of AIS. The first discovery of curcumin exerting neuroprotective effects through epigenetic regulation of ADRB2 expression provides a new strategy for early diagnosis and targeted therapy of AIS, as well as future targeted drugs targeting ADRB2 methylation.

Hypoglossal canal dural arteriovenous fistulas (HCDAVFs) are rare vascular anomalies involving pathological shunts near the hypoglossal canal. Their complex angioarchitecture and variable venous drainage (orbital, posterior fossa or spinal systems) lead to heterogeneous symptoms, such as pulsatile tinnitus and orbital congestion. Diagnosis relies on dynamic digital subtraction angiography (DSA), as noninvasive imaging lacks sensitivity. A single-center retrospective study analyzed 13 HCDAVF patients (2014–2024) with DSA-confirmed diagnosis. Treatment included transvenous embolization (TVE) using detachable coils and Onyx-18, with adjunctive techniques (balloon-assisted flow control). Outcomes were assessed via post-procedural DSA, clinical evaluations, and imaging follow-up. The cohort (10 males, mean age 59.2 years) presented with pulsatile tinnitus (61.5

The neutrophil-to-lymphocyte ratio (NLR) is associated with unfavorable prognosis and hemorrhagic transformation (HT) in patients with ischemic stroke, yet the underlying mechanisms remain unclear. Using patient samples and a murine stroke model, we identified CD8⁺ regulatory T cells (CD8 Tregs) key regulators of neutrophil homeostasis after ischemic stroke, thereby limiting endothelial disruption and HT. Loss of CD8 Tregs expanded circulating neutrophils by extending their lifespan rather than altering proliferation, bone marrow release, or direct cytotoxicity. Mechanistically, CD8 Tregs shortened neutrophil lifespan by modulating HIF-1α-dependent glycolytic activity and relieving PD-L1-mediated suppression of bone marrow clearance. Finally, co-culture experiments with human CD8 Tregs and neutrophils revealed similar neutrophil-regulatory effects, accompanied by improved endothelial barrier integrity. These findings reveal a previously unrecognized CD8 Treg-neutrophil axis and suggest potential therapeutic strategies for preventing HT after stroke.

The apelin/APJ system has garnered increasing attention in recent years. In this review, we comprehensively discuss the physiological and pathological mechanisms of the apelin/APJ system in stroke. The apelin/APJ system is widely expressed in the central nervous system (CNS). However, the distribution of the apelin/APJ system varies across different regions and subcellular organelles of the brain. Additionally, the neuroprotective effects of the apelin/APJ system have been reported to inhibit oxidative and nitrative stresses via various signaling pathways. Despite this, the clinical application of the apelin/APJ system remains distant, as apelin has numerous active forms and signaling pathways. The development of a range of drugs targeting the apelin/APJ system holds promise for treating stroke.

Objective: Deep brain stimulation (DBS) targeting the lateral habenula (LHb) is a promising therapy for treatment-resistant depression (TRD) but its clinical effect has been variable, which can be improved by adaptive DBS (aDBS) guided by a neural biomarker of depression symptoms. Existing neural biomarkers, however, cannot simultaneously track slow and fast symptom dynamics, do not sufficiently respond to stimulation parameters, and lack neurobiological interpretability, which hinder their use in developing aDBS. Methods: We conducted a study on one TRD patient who achieved remission following a 41-week LHb DBS treatment, during which we assessed slow symptom variations using weekly clinical ratings and fast variations using daily self-reports. We recorded daily LHb local field potentials (LFP) concurrently with the reports during the entire treatment process. We then used machine learning methods to identify a personalized depression neural biomarker from spectral and temporal LFP features. Results: The neural biomarker was identified from classification of high and low depression symptom states with a cross-validated accuracy of 0.97. It further simultaneously tracked both weekly (slow) and daily (fast) depression symptom variation dynamics, achieving test data explained variance of 0.74 and 0.63 respectively and responded to DBS frequency alterations. Finally, it can be neurobiologically interpreted as indicating LHb excitatory and inhibitory balance changes during DBS treatment. Conclusion: By collecting and analyzing a unique personalized dataset of weekly and daily LFP recordings and symptom evaluations, we identified a high-performance neural biomarker for depression during LHb DBS. Significance: Our results hold promise to facilitate future aDBS for treating TRD.

Mounting evidence has demonstrated that the transcriptional coactivators Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), are the main effectors of the Hippo signal transduction pathway that is involved in multiple layered events in tumorigenesis. The role of YAP/TAZ in cancer development is critical in a context dependent manner. Overexpression of YAP/TAZ induces cell proliferation and is elevated in various cancers and many other malignancies. On the other hand, studies have shown YAP binds p73 to activate PML transcription in response to DNA damage and generate a DNA-damage-induced feedback loop. Intriguingly, at the genomic level, YAP/TAZ genes are rarely mutated in cancer, except in specific tumors. The central role of YAP/TAZ in driving tumorigenesis is attributed through diverse mechanisms, such as regulatory kinases, cellular mechano-transduction, epigenetic modification/alterations, post-translational modifications, protein -protein interaction and nucleo-cytoplasmic export import. The complex interplay among feedback loops and crosstalk between various signaling pathways portrays the dynamic nature of YAP/TAZ. Thus, a comprehensive understanding of how posttranslational modifications and nucleo-cytoplasmic traffic of YAP/TAZ dynamically regulate and control each other holds great promise for selectively targeting YAP/TAZ import and export for drug therapy.

The histopathological neurons in the brain tissue of drug-resistant epilepsy exhibit aberrant cytoarchitecture and imbalanced synaptic circuit function. However, the gene expression changes of these neurons remain unknown, making it difficult to determine the diagnosis or to dissect the mechanism of drug-resistant epilepsy. By integrating whole-cell patch clamp recording and single-cell RNA-seq approaches, we identified a transcriptionally distinct subset of cortical pyramidal neurons. These neurons highly expressed genes CDKN1A (P21), CCL2, and NFKBIA, which associate with mTOR pathway, inflammatory response, and cellular senescence. We confirmed the expression of senescent marker genes in a subpopulation of cortical pyramidal neurons with enlarged soma size in the brain tissue of drug-resistant epilepsy. We further revealed the expression of senescent cell markers P21, P53, COX2, γ-H2AX, and β-Gal, and reduction of nuclear integrity marker Lamin B1 in histopathological neurons in the brain tissue of patients with drug-resistant epilepsy with different pathologies, but not in control brain tissue with no history of epilepsy. Additionally, chronic, but not acute, epileptic seizures induced senescent marker expression in cortical neurons in mouse models of drug-resistant epilepsy. These results provide important molecular markers for histopathological neurons and what we believe to be new insights into the pathophysiological mechanisms of drug-resistant epilepsy.

AIMS:Sustained neuroinflammation following ischemic stroke impedes post-injury tissue repairment and neurological functional recovery. Developing innovative therapeutic strategies that simultaneously suppress detrimental inflammatory cascades and facilitate neurorestorative processes is critical for improving long-term rehabilitation outcomes. METHODS:We employed a microglia depletion-repopulation paradigm by administering PLX5622 for 7 days post-ischemia; followed by a 7-day withdrawal period to allow microglia repopulation. Single-cell transcriptomics, behavioral testing, cytokine arrays, flow cytometry, and immunofluorescence were used to assess the effects of microglia repopulation and delineate the transition of reshaped immune microenvironment. RESULTS:PLX5622 administration reshaped the poststroke immune microenvironment, promoting neurofunctional recovery. Repopulated microglia adopted a homeostatic phenotype, increasing homeostatic states by ~14.36% and reducing pro-inflammatory states by ~20.17%. This reshaped environment suppressed T cell exhaustion, limited neutrophil terminal differentiation, and promoted a phagocytic macrophage phenotype. Furthermore, we identified that these transitions in infiltrating immune cells may be driven by reduced chemokine production, enhanced blood-brain barrier (BBB) integrity, and transcriptional reprogramming. CONCLUSION:Transient microglial depletion and repopulation via PLX5622 during the acute phase post stroke facilitate the recovery of neurological function. This immunomodulatory strategy offers a promising and clinically translationally relevant approach to enhance functional recovery following ischemic brain injury.

Ischemic stroke is a leading cause of mortality worldwide, with an excessive immune response playing a major role in exacerbating post-stroke pathogenesis. Regulatory T (Treg) cells, known for their immunosuppressive properties, are believed to be crucial in mitigating post-stroke inflammation. Moreover, emerging evidence suggests that Treg cells contribute to ischemic stroke recovery by suppressing neurotoxic astrogliosis and by promoting myelination regeneration. However, significant challenges remain before the clinical translation of Treg cell-based therapies can be realized. In this review, we summarize recent advances in understanding the role of Treg cells in ischemic stroke, with a particular emphasis on CD8+ Treg cells, a subset that has been largely overlooked. We comprehensively explore the activation, expansion, recruitment, and functional mechanisms of Treg cells during both the acute and chronic phases of stroke. Additionally, we highlight unresolved challenges and discuss potential strategies for translating Treg-based therapies into clinical application. The development of Treg cell-based treatments holds promise for revolutionizing ischemic stroke therapy, opening new avenues for patient treatment and recovery.

The primate amygdala serves to evaluate the emotional content of sensory inputs and modulate emotional and social behaviors; it modulates cognitive, multisensory and autonomic circuits predominantly via the basal, lateral and central nuclei, respectively. Recent evidence has suggested the mesoscale (millimeter-scale) nature of intra-amygdala functional organization. However, the connectivity patterns by which these mesoscale regions interact with brainwide networks remain unclear. Using infrared neural stimulation of single mesoscale sites coupled with mapping in ultrahigh field 7-T functional magnetic resonance imaging, we have discovered that these mesoscale sites exert influence over a surprisingly extensive scope of the brain. Our findings strongly indicate that mesoscale sites within the amygdala modulate brainwide networks through a 'one-to-many' (integral) way. Meanwhile, these connections exhibit a point-to-point (focal) topography. Our work provides new insights into the functional architecture underlying emotional and social behavioral networks, thereby opening up possibilities for individualized modulation of psychological disorders.

Pituitary adenomas (PAs) are common intracranial tumors whose mass effects and endocrine dysfunction pose serious threats to patient health. However, the mechanisms underlying their progression, particularly the role of the tumor microenvironment (TME), remain insufficiently studied. Within this context, cancer-associated fibroblasts (CAFs) have been shown to drive tumor development via extracellular matrix remodeling and extracellular vesicle release, but their specific contributions to PA progression remain unclear. In this study, we observed a correlation between PA invasiveness and fibroblast density in the TME. Functionally, both CAFs and CAF-derived exosomes significantly enhanced the proliferation and invasion of PA cells compared to normal fibroblasts. Small RNA sequencing identified 16 upregulated and 8 downregulated miRNAs in CAF-derived exosomes, with KEGG analysis indicating enrichment in MAPK signaling, regulation of actin cytoskeleton, and lysosome-related pathways. Among these, miR-184 was notably upregulated in both CAF-derived exosomes and PA specimens. We further demonstrated that exosomal miR-184 from CAFs could be transferred into PA cells, promoting their proliferation and invasion, while miR-184 knockdown attenuated the tumor-promoting effects of CAF-derived exosomes. Mechanistically, TLE1 was validated as a direct functional target of miR-184. In summary, our study reveals exosomal miR-184 as a key mediator of CAF-driven PA progression, highlighting its potential as a therapeutic target for PAs.