Chongqing Medical University

Photodynamic therapy (PDT) has emerged as a promising noninvasive treatment for cancer and other diseases. Aggregation‐induced emission (AIE) photosensitizers are excellent candidates for enhancing the efficacy of image‐guided PDT due to their unique properties. DNA‐modified AIE luminogens (AIEgens) offer an effective approach for nucleic acid detection and biospecies sensing, but their applications in tumor cell imaging and image‐guided PDT have been rarely reported. Herein, we designed a light‐up probe, named ApApt, for targeted imaging and image‐guided PDT of cancer cells. The probe was prepared by conjugating AIEgen with aptamer and displayed specific targeting ability to EpCAM‐positive cancer cells. ApApt exhibits good water solubility and shows very low emission in aqueous solution. However, it emits strong fluorescence as a result of the restricted intramolecular motion activation of AIEgens, which is triggered by the specific binding between the aptamer SYL3C and EpCAM protein. Upon delivery to cancer cells, ApApt efficiently generates ROS for targeted PDT under light irradiation.

Allogeneic hematopoietic stem cell transplantation (allo‐HSCT) is pivotal for hematological malignancies but faces challenges in delayed platelet engraftment, poor graft function (PGF), and bleeding risks. Hetrombopag, a thrombopoietin receptor agonist, was evaluated to enhance platelet recovery posttransplant. Patients undergoing allo‐HSCT were randomized on Day 3 Post‐Infusion into low‐dose (2.5 mg/day), high‐dose (5 mg/day) hetrombopag groups, or a control group receiving thrombopoietin (300 U/kg/day). Endpoints included platelet/neutrophil engraftment time, PGF incidence, transfusion needs, and safety. Among 212 analyzed patients, platelet engraftment was faster in hetrombopag groups (median 13 days) versus controls (15 days; p = 0.001), with no dose‐dependent difference (p = 0.821). Neutrophil engraftment was also accelerated (13 vs. 15 days; p = 0.002). PGF incidence was lower in hetrombopag groups (5.04%) versus controls (13.7%; p = 0.042). The experimental group required fewer platelet transfusions (p = 0.021), had reduced gastrointestinal bleeding, and lower costs. Secondary platelet recovery failure showed no intergroup differences. Hetrombopag safely accelerates platelet and neutrophil engraftment, reduces PGF risk, and decreases transfusion dependency post‐allo‐HSCT. Low‐dose hetrombopag demonstrated efficacy equivalent to high‐dose, offering a cost‐effective strategy to improve transplant outcomes. Trial Registration: ChiCTR2200057764.

Background The global burden and trend of musculoskeletal disorders (MSDs) in postmenopausal women (PMW) remain unclear. Methods Using the Global Burden of Disease (GBD) 2021 data, this study assessed the prevalence and disability-adjusted life years (DALYs) for rheumatoid arthritis (RA), osteoarthritis (OA), low back pain (LBP), neck pain (NP), gout, and other musculoskeletal conditions (OMSKDs) from 1990 to 2021. Bayesian Age-Period-Cohort (BAPC) models projected trends to 2045. Health inequalities were analyzed using the Slope Index of Inequality (SII) and the Concentration Index, with decomposition methods identifying the drivers of burden changes. Results From 1990 to 2021, the age-standardized prevalence and DALYs rates have significantly increased among PMW, with OA and LBP being the primary contributors to this burden. These increases were primarily driven by population growth. Specifically, RA, OA, and gout accounted for more than 50% of the total burden in women across all age groups, with RA burden being 1.2 times higher than that in premenopausal women, OA 3.1 times higher, and gout 2.9 times higher. Notably, in PMW, the burden of gout was 74%. The burden of gout is strongly correlated with the Socio-Demographic Index (SDI), particularly in high-income regions, such as North America, where the United States exhibits the highest DALYs rates. Furthermore, projections indicate that by 2045, the global burden of MSDs could double, with OA potentially affecting nearly 50% of the PMW. Conclusion From 1990 to 2021, the global burden of MSDs among PMW has risen significantly, with notable regional disparities underscoring the critical need for tailored preventive strategies to alleviate the worldwide impact of these conditions.

Peri-implant keratinized mucosa (PIKM) augmentation refers to surgical procedures aimed at increasing the width of PIKM. Consensus reports emphasize the necessity of maintaining a minimum width of PIKM to ensure long-term peri-implant health. Currently, several surgical techniques have been validated for their effectiveness in increasing PIKM. However, the selection and application of PIKM augmentation methods may present challenges for dental practitioners due to heterogeneity in surgical techniques, variations in clinical scenarios, and anatomical differences. Therefore, clear guidelines and considerations for PIKM augmentation are needed. This expert consensus focuses on the commonly employed surgical techniques for PIKM augmentation and the factors influencing their selection at second-stage surgery. It aims to establish a standardized framework for assessing, planning, and executing PIKM augmentation procedures, with the goal of offering evidence-based guidance to enhance the predictability and success of PIKM augmentation.

Purpose The aim of this study was to assess the outcomes and risk factors for in-hospital mortality and further explore a predictive model for forecasting in-hospital mortality in HIV-positive patients with sepsis. Methods A retrospective cohort study of 203 hospitalized HIV-positive patients with sepsis was conducted at Chongqing Public Health Medical Center, a tertiary-level infectious disease hospital, from January 2021 to December 2023. Patients were divided into two groups according to survival status (survival and death). The patients’ baseline characteristics, laboratory findings and outcomes were collected for comprehensive analysis. Results The in-hospital mortality rate was 18.7%. Independent risk factors for in-hospital mortality in HIV-positive patients with sepsis were acute respiratory failure (OR 3.654, 95% CI 1.303–10.248, p = 0.014), septic shock (OR 9.542, 95% CI 3.614–25.197, p < 0.001), chronic liver disease (OR 4.330, 95% CI 1.348–13.910, p = 0.014) and lactate (OR 1.570, 95% CI 1.195–2.062, p = 0.001). The AUC for the RF model to predict in-hospital death was 0.853, and the threshold was −1.553 with a sensitivity of 73.7% and a specificity of 84.8%. Conclusions Acute respiratory failure, septic shock, chronic liver disease and lactate were independent risk factors for in-hospital mortality in HIV-positive patients with sepsis. The prediction model based on these four risk factors demonstrated good effectiveness in predicting in-hospital mortality among HIV-positive patients with sepsis.

Hydrogels, as three‐dimensional hydrophilic polymer networks, have been widely utilized in biomedical applications due to their excellent biocompatibility, high water content, and tunable physicochemical properties. However, traditional bulk hydrogels often suffer from limitations such as inadequate mechanical strength, slow response to external stimuli, and restricted diffusion efficiency, which hinder their performance in dynamic biological environments. To overcome these challenges, hydrogel microspheres (HMs) have emerged as a promising alternative, which offers advantages such as injectability, high surface‐area‐to‐volume ratio, and tunable functionality. By integrating natural and synthetic materials with advanced fabrication techniques, including microfluidics and emulsification, researchers have achieved precise control over the morphology, size, and bioactivity of HMs. In recent years, stimuli‐responsive HMs have attracted significant attention for their ability to respond intelligently to environmental cues such as pH, reactive oxygen species (ROS), enzymes, and temperature. This enables controlled drug release, enhanced therapeutic precision, and spatiotemporal regulation in biomedical applications. This review systematically summarizes the materials, fabrication strategies, and functional mechanisms of stimuli‐responsive HMs, highlighting their applications in drug delivery, disease treatment, and tissue engineering. Furthermore, key challenges and future perspectives are discussed, which provides insights into how these intelligent HMs can advance personalized medicine and clinical translation.

Background Noninvasive ventilation (NIV) is frequently employed for acute hypoxemic respiratory failure, yet optimal intubation timing for high-risk NIV failure patients remains uncertain. Objectives To investigate mortality outcomes associated with early versus late intubation in high-risk NIV failure patients. Design Secondary analysis of a multicenter observational cohort study. Methods Patients with high NIV failure risk (updated HACOR score ⩾11 after 1–2 h of NIV) were enrolled. We defined that intubation was needed in these high-risk patients. Intubation occurring within 12 h of NIV initiation was classified as early intubation, while intubation after 12 h was designated as late intubation. Primary outcomes were intensive care unit (ICU) and hospital mortality. In sensitivity analyses, patients who achieved NIV success were categorized into the late-intubation group. Due to baseline imbalances, propensity score matching was performed with covariate adjustment. Results Among the study population, 171 patients underwent early intubation and 222 underwent late intubation. Despite greater baseline severity in the early intubation group, ICU mortality (36% vs 58%, p < 0.001) and hospital mortality (38% vs 58%, p < 0.001) were significantly lower compared to the late-intubation group. In sensitivity analyses, 190 patients with NIV success were included in the late-intubation group, further accentuating the severity disparity between groups. After propensity matching (220 patients: 110 per group), most of the baseline characteristics were comparable. The early intubation group had a 100% intubation rate versus 71% in the late-intubation group, with the latter exhibiting higher mortality (ICU: 46% vs 32%, p = 0.052; hospital: 50% vs 34%, p = 0.020). Conclusion In patients at high risk for NIV failure, early intubation is associated with reduced mortality.

Background Metabolic factors are considered to influence disease progression in patients with Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), but the impact of individual metabolic factors on the survival rate of patients with MASLD is still unclear. Aims This article aims to reveal how metabolic components affect the survival of patients with this disease. Methods A total of 3,086 participants with MASLD based on the diagnostic criteria established at the Delphi conference from NHANES III were included in this analysis. COX regression model (C-index = 0.64) was used to analyze the all-cause and attributable mortality of different number of metabolic factors. Elastic Network Regression model (C-index = 0.69), Accelerated Failure Time model and Randomized Survival Forest model (C-index = 0.63) based on machine learning were used to analyze the weight of each metabolic factor, and a Metabolism-related survival risk score formula was established and verified. Results This study found that not only the number of metabolic factors had different effects on all-cause survival in MASLD patients, but also the degree of impact of different metabolic factors on survival was quite different, among which poor glycemic control was the most important influencing factor. Conclusion This study highlights the clinical value of relevant metabolic factors in predicting survival in the MASLD patient population. Related metabolic factors can be used as surrogate biomarkers for the follow-up of MASLD patients.

Background Acute myeloid leukemia (AML) with nucleophosmin 1 (NPM1) mutations represents a distinct subtype of leukemia. Emerging evidence suggests that regulation of redox metabolism contributes to tumorigenesis and reveals a metabolic vulnerability in anti-tumor therapies. However, the role of redox homeostasis between reactive oxygen species (ROS) and antioxidant systems plays in NPM1-mutated AML has not been fully elucidated. Methods First, ROS-related metabolic pathways in NPM1-mutated AML were analyzed using RNA-sequencing data. Intracellular and mitochondrial ROS levels in leukemia cells were detected using flow cytometry (FCM). The expression of nuclear factor (erythroid-derived 2)-like 2 (NRF2) was analyzed in public databases and further validated in AML primary blasts and cell lines by quantitative real-time PCR (qRT-PCR), western blotting, and immunofluorescence. Next, the mechanism underlying NRF2 expression was investigated through the RNA immunoprecipitation (RIP), methylated RNA immunoprecipitation (MeRIP) and rescue experiments. Additionally, the downstream target gene of NRF2 was identified by bioinformatics analysis and chromatin immunoprecipitation (ChIP) assays. Furthermore, RNA interference and the NRF2 inhibitor ML385 were applied to explore the role of NRF2 in leukemia. Finally, the anti-leukemic effects of ML385 alone or in combination with the B-cell lymphoma 2 (BCL-2) inhibitor venetoclax on AML cells were investigated using FCM analysis and western blotting, and further explored in cell line-derived xenograft (CDX) mouse models. Results In this study, we identified significant ROS accumulation in leukemia cells with NPM1 mutations. Meanwhile, elevated NRF2 expression and its nuclear localization were observed in NPM1-mutated AML cells. The high NRF2 expression levels were at least partially induced by fat mass and obesity-associated protein (FTO) via m⁶A modification. Functionally, NRF2 exerts its antioxidant effects by transcriptionally upregulating malic enzyme 1 (ME1) expression and enhancing its activity. Targeting NRF2/ME1 axis reduced NADPH/NADP⁺ ratio, increased ROS levels, impaired leukemia cell viability, and promoted apoptosis. More importantly, NRF2 inhibitor ML385 in combination with venetoclax showed synergistic anti-leukemic activity in vitro and in vivo. Conclusion Overall, our findings provide new insight into the therapeutic potential of targeting NRF2 and guide the development of innovative combination therapies in NPM1-mutated AML.

Background. This study aims to investigate the association between carbon monoxide (CO) and blood pressure (BP), which may be mediated by lipid metabolites. Methods. This study utilized data from the Health Cohort Study of Children and Adolescents in Chongqing, China. The absolute quantification of lipid profiling was performed using ultra-high-performance liquid chromatography tandem mass spectrometry. The data on outdoor CO was sourced from the China High Air Pollution dataset. Results. A total of 3,121 children were included. CO exposure was positively correlated with changes in systolic BP (β = 1.67; 95%CI: 0.80, 2.53; P = 0.001) and diastolic BP (β = 0.96; 95%CI: 0.26, 1.66; P = 0.007). Phosphatidylethanolamine (PE) (P-18:0/22:5) and triglyceride (TG) (17:1_17:1_13:0) may play a mediating role between CO and systolic BP changes, while lysophosphatidylcholine (LPC) (22:0), phosphatidylcholine (PC) (38:6), PC(O-21:2), phosphatidylserine (PS) (18:0/20:4), and sphingomyelin (SM) (d21:1) may mediate the relationship between CO and diastolic BP changes. The enrichment analysis indicated that CO exposure may primarily affect lipid metabolites related to acetylcholine synthesis, phospholipid biosynthesis, and phosphatidylcholine catabolism. Conclusion. CO exposure is positively correlated with changes in both systolic and diastolic BP in children. Additionally, lipid metabolites partly mediate the relationship between CO and changes in BP.

Purpose To comprehensively evaluate the efficacy and safety of combining poly (ADP-ribose) polymerase (PARP) inhibitors with chemotherapy in patients with advanced breast cancer. Methods A systematic literature search was conducted in PubMed, Embase, Cochrane Library, Web of Science, and ClinicalTrials.gov to identify randomized controlled trials (RCTs) evaluating PARP inhibitor-chemotherapy combinations. Studies reporting progression-free survival (PFS), overall survival (OS), overall response rate (ORR), and safety outcomes were included. Data extraction and quality assessment were performed independently by two reviewers, and a meta-analysis was conducted using random-effects models. Results Of 970 studies retrieved, four RCTs involving 1064 patients met the inclusion criteria. PARP inhibitors combined with chemotherapy significantly improved PFS (hazard ratio [HR] 0.73, 95% confidence interval [CI] 0.63-0.84, P < .0001) and showed a trend towards improved OS (HR 0.93, 95% CI 0.79-1.09, P = .36), though this was not statistically significant. There was no significant improvement in ORR (RR 1.08, 95% CI 0.98-1.20, P = .13). Regarding safety, no significant difference was observed in all grades or grade 3-4 adverse events (AEs) overall, but the combination therapy was associated with an increased risk of anemia, nausea, and diarrhea (RRs ranging from 1.14 to 1.29, all P < .01). Conclusion PARP inhibitor combined with chemotherapy is an effective option for the treatment of patients with advanced breast cancer, but its potential increased risks of specific AEs need to be weighed. Clinicians should make individualized treatment plans according to the specific conditions of patients, comprehensive consideration of efficacy and safety.

Background Pre‐pregnancy obesity significantly impacts maternal and perinatal health, being linked to various adverse pregnancy outcomes (APOs). While studies have observed an association between obesity and certain pregnancy complications, causality remains unclear. The pathophysiological mechanisms linking obesity to increased pregnancy risks are still under investigation. Clarifying these mechanisms may help to identify additional biomarkers for the accurate prediction and prevention of specific APOs in pre‐pregnant individuals with obesity. Methods In this investigation, we employed Mendelian randomization (MR) analysis utilizing data from the UK Biobank and FinnGen datasets to discern the genetic causal association between pre‐pregnancy obesity and 23 APOs. A two‐step MR approach was applied to elucidate the mediating and pathophysiological pathways through which obesity elevates the risk of pregnancy‐related complications. Results Our findings reveal a significant causal association between pre‐pregnancy obesity and pregnancy hypertension (HP), pre‐eclampsia/eclampsia (PE/E), and gestational diabetes (GDM). Mediation analysis further identified triglycerides, circulating leptin levels, fasting insulin, and interleukin‐6 levels as key factors mediating the partial causal effects of maternal obesity on HP and GDM. It was also found that there was no causal association between pre‐pregnancy obesity and certain pregnancy complications (e.g., preterm labor, postpartum hemorrhage, and postpartum depression), but this does not preclude there being a correlation between the two. Conclusion Obesity does not directly affect all APOs. Insulin resistance, lipotoxicity, and inflammation mediate the causality between obesity and certain pregnancy‐related conditions and may promote the prediction and prevention of specific APOs.

Myocarditis is a leading cause of sudden cardiac death and dilated cardiomyopathy in young adults, and effective therapies are urgently needed. Here, it is found that intravenous transplantation of exogenous mitochondria (Mito) significantly attenuates inflammation and oxidative stress in the heart, mitigates myocardial injury, improves cardiac function, and alleviates fibrosis and heart failure in mice with experimental autoimmune myocarditis (EAM). Mechanistically, injected Mito can be internalized by neutrophils and subsequently transported to the inflamed hearts of EAM mice. Following internalization in neutrophils, Mito may induce mitochondrial fusion, restore mitochondrial function, inhibit the mitochondrial permeability transition pore opening, and reduce excessive production of mitochondrial reactive oxygen species. These effects collectively inhibit NETosis, known as the formation of neutrophil extracellular traps (NETs), thereby suppressing inflammation and apoptosis of cardiomyocytes induced by NETs. Notably, these findings demonstrate for the first time that mitochondrial transplantation exert therapeutic effects by regulating neutrophils rather than directly integrating into target cardiomyocytes. Additionally, a combination therapy is developed by engineering Mito with a novel bifunctional peptide possessing anti‐inflammatory and anti‐fibrotic properties, which shows potent synergistic effects in treating myocarditis in mice. This findings provide a new strategy toward innovative mitochondrial‐derived therapies for myocarditis and other autoimmune and inflammatory diseases.

Conventional tumor therapies typically depend on the apoptotic pathway, which often leads to inadequate immunogenicity. This limitation underscores the urgent need for innovative treatments that enhance immunogenicity. In this study, an ultrasound (US)‐activated nano‐oncolytic system (designated as cRGD‐Lip@PFP), is presented and consists of nanoliposomes (Lip) modified with the cRGD peptide for targeted tumor delivery. This system features a perfluoropentane (PFP) core that undergoes US‐triggered acoustomechanical effects, enabling controlled expansion from nanoscale to microscale, ultimately leading to rupture and the generation of cavitation effects. Intracellular cavitation further induces necroptosis‐like oncolytic cell death. The efficacy of various treatments in stimulating immune responses is systematically compared and it is demonstrated that the nano‐oncolytic system effectively enhances the release of damage‐associated molecular patterns (DAMPs). Additionally, the release of DNA fragments activates the cGAS‐STING pathway, resulting in an amplified immune response. Furthermore, this nano‐oncolytic system alleviates the hypoxic tumor microenvironment and counteracts immunosuppression. Compared to traditional apoptosis, the necroptosis‐like oncolytic cell death induced by this strategy exhibits enhanced immunogenicity. This approach presents an innovative paradigm for tumor immunotherapy based on acoustomechanical effects, offering a promising alternative to tackle the issue of insufficient immunogenicity often associated with conventional apoptosis therapies.

Background Metabolic-associated fatty liver disease (MAFLD) is a growing global health concern, particularly among women of childbearing age (WCBA). We aimed to analyze the global burden of MAFLD among WCBA from 1990 to 2021 and project trends to 2040. Methods Data on incidence, prevalence, deaths, and disability-adjusted life years (DALYs) were extracted from the Global Burden of Disease Study 2021. Joinpoint regression and decomposition analysis were used to assess historical trends, and Bayesian Age-Period-Cohort (BAPC) modeling projected future burdens. Results From 1990 to 2021, the age-standardized rate (ASR) of MAFLD incidence and prevalence among WCBA increased globally (EAPC = 0.76 and 0.71, respectively). China showed declining trends in deaths (EAPC = −2.63) and DALYs (EAPC = −2.62). By 2040, BAPC modeling predicts a continued rise in global incidence and prevalence, with regional disparities in mortality. Population growth was the primary driver of the global increase in MAFLD incidence, accounting for 63.38% of the rise. Conclusion MAFLD imposes a significant burden on WCBA globally, with socioeconomic disparities driving regional variations. Targeted interventions addressing obesogenic environments and healthcare inequities are urgently needed.

Objective We aimed to evaluate the incidence of and risk factors for mortality in children with mushroom poisoning. Methods Sixty-seven children with mushroom poisoning who were hospitalized at the Children’s Hospital of Chongqing Medical University were retrospectively enrolled. The clinical characteristics of the children in the surviving and non-surviving groups were compared. Variables with a P value < 0.1 in the univariate logistic regression analysis were included in the multivariate logistic regression analysis. A receiver operating characteristic (ROC) curve was generated to determine the optimal cutoff point. Results The mortality rate of children with mushroom poisoning was 23.88% (16/67), and the incidence of death during hospitalization was 35.02 per 1,000 person-days. The median pediatric sequential organ failure assessment (pSOFA) score was 1.00 (interquartile range [IQR] 0.00–3.00). Logistic regression analysis revealed that the pSOFA score was independently associated with mortality (odds ratio [OR] 4.92, 95% confidence interval [CI] 1.59–62.21; P = 0.040). The optimal cutoff point of the pSOFA score for predicting mortality was 2.00, with an area under the curve (AUC) of 0.84 (95% CI 0.71–0.88, P < 0.001*). Conclusions In this study, the incidence of death among children with mushroom poisoning was retrospectively evaluated. The pSOFA score may serve as a good prognostic indicator in children with mushroom poisoning, and children with a pSOFA score ≥ 2 have a significantly increased risk of mortality.

Hepatocellular carcinoma (HCC) is the prevalent form of primary liver cancer with a high rate of morbidity and death. Ferroptosis is a kind of regulatory cell death mode that depends on iron. Small ubiquitin-like modifier 2 (SUMO2) is linked to HCC progression; however, its role in ferroptosis within HCC remains unclear. Our goal was to evaluate the regulatory effects and molecular mechanisms of SUMO2 in HCC ferroptosis. SUMO2 was screened by bioinformatics analysis, and its expression was verified in HCC tissues. Stable SUMO2 knockdown and overexpression cell lines were created. The downstream target protein acyl-CoA synthetase long-chain family member 3 (ACSL3) of SUMO2 was screened to assessed the mechanism of SUMO2 regulating ferroptosis in HCC cells. In HCC tissues, SUMO2 expression was higher and linked to a worse prognosis for patients. SUMO2 overexpression reduced malondialdehyde content, prevented mitochondrial crest loss, and increased glutathione level under ferroptotic stimuli. Meanwhile, overexpression of SUMO2 lowered the expression of molecules that promote ferroptosis and raised the expression of molecules that prevent it. SUMO2 knockdown produced the opposite effects. Mechanistically, SUMO2 elevated ACSL3 protein level by inhibiting its entry into the ubiquitin–proteasome degradation pathway and enhanced its protein stability. The inhibitory effects of SUMO2 on ferroptosis in HCC cells were reversed by ACSL3 knockdown in SUMO2-overexpressing cells. In summary, SUMO2 binds to ACSL3, preventing its protein degradation, thereby increasing its protein stability and level, which in turn negatively regulates ferroptosis in HCC cells. These results point to interesting targets and therapeutic approaches for HCC. Supplementary Information The online version contains supplementary material available at 10.1007/s12672-025-02921-5.

The blood–brain barrier (BBB) acts as a stringent biological filter situated between the circulatory system and the brain's tissue, shielding the brain by preventing the entry of detrimental neurotoxic substances into the central nervous system (CNS). Nevertheless, the BBB also restricts the entry of most therapeutic drugs, resulting in only a few medications currently available for the clinical treatment of neurological diseases. Consequently, it is imperative to discover a secure and potent technique to temporarily disrupt the BBB for the purpose of directed medication administration. The therapeutic approach of ultrasound‐induced BBB opening combined with drug delivery offers advantages such as non‐invasiveness, precise targeting, and deep tissue penetration. It overcomes the limitations of traditional therapies blocked by the BBB and shows significant potential for treating neurological disorders. This review includes an overview of the physical characteristics and transport mechanisms of the BBB, followed by an introduction to the mechanisms of ultrasound‐mediated BBB opening. Additionally, it summarizes the neural and immune regulation following BBB opening by ultrasound, with a focus on its features and clinical applications in immunotherapy. These extensive insights aim to provide promising strategies for the clinical application of ultrasound‐mediated BBB opening for targeted and personalized drug delivery.