Neovascular age-related macular degeneration (nAMD) is a major cause of irreversible vision impairment in elderly populations, characterized by pathological angiogenesis beneath the macula. Although anti-VEGF therapies have demonstrated clinical effectiveness, significant challenges including drug resistance and the need for frequent intravitreal injections persist. As natural nanovesicles, exosomes derived from mesenchymal stem cell (MSC) can mediate intercellular communication, making them an attractive alternative for modulating cellular processes. This study explored the anti-angiogenic effects of MSC-derived exosomes in nAMD, with particular emphasis on the role of a specific exosomal lncRNA lnc-AGT-3. Our results showed that lnc-AGT-3 expression was reduced in both nAMD patients and choroidal neovascularization (CNV) models, and its overexpression effectively inhibited pathological angiogenesis in vitro and in vivo. Mechanistically, lnc-AGT-3 enhanced the p53 signaling pathway by blocking the ubiquitination and degradation of p53 and ultimately inhibited neovascularization, a process potentially linked to its direct interaction with heterogeneous nuclear ribonucleoprotein K (hnRNP K). Our findings position MSC-derived exosomes enriched with lnc-AGT-3 as an innovative therapeutic paradigm for nAMD, acting through p53 pathway modulation to potentially overcome current treatment limitations.

Neovascular age-related macular degeneration (nAMD) and proliferative diabetic retinopathy (PDR), though clinically distinct, are both sight-threatening ocular disorders driven by pathological neovascularization. However, their shared molecular mechanisms remain poorly characterized. In this study, we performed DIA quantitative proteomic analysis of aqueous humor (AH) from patients with nAMD, PDR, and control. A total of 3186 proteins were identified, in which 877 and 1,017 differentially expressed proteins (DEPs) were detected in the nAMD and PDR groups, respectively, compared to control group. Functional enrichment analysis revealed significant involvement of inflammatory and metabolic pathways in both diseases. Notably, the persistent upregulation of cell division cycle 42 (CDC42) and ras homolog family member A (RHOA) in nAMD and PDR, combined with their established role in cytoskeletal remodeling, suggests their significant involvement in pathological angiogenesis. These findings offer novel perspectives on shared pathogenic pathways in neovascular ocular disorders and suggest potential therapeutic targets for further investigation.

Wet age-related macular degeneration (wAMD) is a leading cause of irreversible vision loss characterized by pathological choroidal neovascularization (CNV). While anti-VEGF therapies are the standard of care, limitations such as treatment resistance and side effects necessitate novel therapeutic agents. This study evaluates the therapeutic efficacy and mechanism of EV30, a novel pterostilbene derivative, in suppressing CNV. EV30 was synthesized based on the pterostilbene template. In vitro, the effects of EV30 on human umbilical vein endothelial cells (HUVECs) proliferation, migration, and tube formation were assessed using Cell Counting Kit-8 (CCK-8), scratch wound, and tube formation assays, respectively. Mechanistic pathways were investigated via Western blotting and RT-qPCR. In vivo, a laser-induced CNV mouse model was treated with intravitreal EV30. Efficacy was evaluated utilizing fundus photography, fluorescein angiography (FFA), optical coherence tomography (OCT), and choroidal flat mounts (IB4 staining). Finally, biosafety was assessed through histology (H&E), electroretinography (ERG), and blood analysis. EV30 demonstrated potent anti-angiogenic properties in vitro, significantly inhibiting HUVEC proliferation, migration, and tube formation in a dose- and time-dependent manner. EV30 reduced vascular endothelial growth factor A (VEGFA) expression and modulated the phosphorylation status of proteins associated with the mTOR/NF-κB/p38 MAPK signaling pathway. In the laser-induced CNV model, EV30 effectively reduced lesion area and vascular leakage comparable to bevacizumab. Furthermore, ERG analysis revealed that EV30 partially preserved retinal electrophysiological function, as indicated by improved scotopic a-wave amplitudes, suggesting functional protection of the retina in the CNV model. EV30 exerted anti-angiogenic effects and was associated with modulation of mTOR/NF-κB/p38 MAPK signaling activity. Together, these findings suggest that EV30 represents a potential therapeutic candidate for CNV by suppressing pathological angiogenesis and modulating inflammation-associated signaling pathways.

BackgroundResponse to secukinumab in psoriasis varies over time and is not fully captured by single timepoint endpoints. Baseline features associated with long-term response trajectories remain unclear.ObjectiveTo identify 52-week secukinumab response trajectories and examine baseline clinical and peripheral blood mononuclear cell (PBMC) transcriptomic features associated with divergent trajectories.MethodsWe analyzed 485 secukinumab-treated patients with plaque psoriasis from the Shanghai Psoriasis Effectiveness Evaluation CoHort (SPEECH). Latent class mixed models were used to derive 52-week Psoriasis Area and Severity Index (PASI) trajectories. Baseline factors associated with the suboptimal trajectory were assessed by logistic regression. In an exploratory subset of 27 patients, paired PBMC samples collected at baseline and week 4 underwent bulk RNA sequencing.ResultsTwo PASI trajectories were identified: an optimal trajectory (432/485, 89.1%) with rapid, sustained improvement and a suboptimal trajectory (53/485, 10.9%) with higher disease activity. Higher baseline PASI, body mass index (BMI), prior biologic exposure, multi-seasonal flare pattern, and infection-triggered flare history were independently associated with the suboptimal trajectory. Week 4 PASI improvement showed moderate discrimination between the two groups. Baseline PBMC transcriptomes also differed, with the optimal trajectory showing a more prominent mature low-density neutrophil signature and a greater reduction in that signature from baseline to week 4.ConclusionLong-term response to secukinumab followed two distinct trajectories. Baseline PASI, BMI, prior biologic exposure, patient-reported flare history, and the mature low-density neutrophil signature may help identify patients with different long-term response patterns.

AIM: To summarize publication trends in the field of strabismus over the past 30y and predict future research hotspots. METHODS: A total of 2915 English-language articles and reviews on strabismus, published between 1993 and 2022, were retrieved from the Web of Science Core Collection. Bibliometric analyses were performed using VOSviewer and CiteSpace software to explore publication trends, as well as the contributions and collaborative networks of countries/regions, authors, institutions, and journals. RESULTS: The annual number of publications on strabismus showed a consistent upward trend. The United States (USA) maintained a leading position in this research field while Republic of Korea and China emerged as rapidly advancing contributors over the last decade. The University of California, Los Angeles ranked as the most productive institution, and Jonathan M. Holmes from USA was the most productive author. Journal of AAPOS was the leading journal with the most strabismus publications, whereas the two most highly cited articles were both published in Ophthalmology. Co-occurrence analysis identified pivotal keywords and burst terms, including intermittent exotropia (IXT), acute acquired comitant esotropia (AACE), functional magnetic resonance imaging (fMRI), and surgical treatment, which were confirmed as predominant and frontier topics. CONCLUSION: This study provides a comprehensive bibliometric analysis of strabismus research, revealing the evolution of research hotspots over the past 30y and outlining several cutting-edge directions for future investigation.

In the era of big data, the rapid expansion of multi-source and multimodal ophthalmic data has created unprecedented opportunities for vision science research. Continuous advances in artificial intelligence (AI) have enabled the efficient processing of large-scale, high-dimensional, and complex datasets, facilitating the discovery of latent patterns and accelerating scientific progress. Despite these advances, ophthalmology continues to face substantial challenges related to data integration, standardization, and effective utilization, and the real-world performance, robustness, and generalizability of AI models in clinical settings remain insufficiently validated. From a data-centric perspective, this review systematically summarizes the fundamental characteristics and scientific value of ophthalmic data, encompassing both imaging and non-imaging modalities. We synthesize recent progress in AI-driven applications for disease screening, diagnostic assistance, prognostic evaluation, and mechanistic exploration. In addition, we critically discuss the opportunities and challenges associated with the integration of AI into ophthalmic clinical practice and basic research, with the aim of providing conceptual insights and future directions for the development of intelligent and data-driven ophthalmic research.

Retinal pigment epithelium (RPE) degeneration is the pathological hallmark of multifactorial dry age-related macular degeneration (dAMD). Mounting evidence implicates oxidative stress and aberrant activation of mammalian target of rapamycin (mTOR) as key drivers of this process. Recent studies have shown that simultaneous modulation of these pathways may offer therapeutic benefit. However, clinical trials of rapamycin, an mTOR inhibitor widely employed in retinal research, have demonstrated limited efficacy, potentially due to poor bioavailability and paradoxical effects on RPE and photoreceptors. To overcome these challenges, APMNP@Rapa, a rapamycin-loaded, methionine-based ROS-responsive polymeric micellar system functionalized with an Ab peptide for active targeting of damaged RPE is developed. The micelles self-assemble from poly(ethylene glycol) - poly-methionine copolymers, leveraging methionine's endogenous nature and innate biocompatibility as an innovative ROS-responsive motif. This design yields particles with exceptional circulation stability and enhanced biocompatibility. In the high-ROS microenvironment of diseased RPE, APMNP@Rapa triggers on-demand rapamycin release. In a sodium iodate (NaIO 3 )-induced RPE oxidative stress model, APMNP@Rapa simultaneously inhibited aberrant mTOR activation, attenuated oxidative damage, and suppressed inflammatory response. These combined effects resulted in a marked preservation of the retina against degradation. Overall, the research establishes a paradigm for intravenous treatment of dAMD using multifunctional nanotherapy.

Intensive medical management has been recommended for ischemic stroke of intracranial atherosclerosis (ICAS), but 9.4–15

Objective To investigate the value of artificial intelligence-assisted compressed sensing(ACS)technology for intravenous gadolinium contrast-enhanced magnetic resonance imaging of the inner ear using three-dimensional fluid-attenuated inversion recovery(3D-FLAIR)sequence.Methods The patients received gadolinium contrast-enhanced magnetic resonance imaging using ACS and united compressed sensing(uCS)3D-FLAIR at Zhongshan Hospital,Fudan University from January to November 2024 were prospectively enrolled.The repetition time was 16000 ms,and acquisition time was 6 min 40 s and 10 min 24 s in ACS 3D-FLAIR and uCS 3D-FLAIR,respectively.The images on the two sequences were evaluated independently by two radiologists.The image quality of the two sequences was subjectively evaluated and compared.The signal-to-noise ratio(SNR)and contrast-to-noise ratio(CNR)were compared between the two sequences.The grading consistencies using two sequences and between the two doctors were analyzed.Results There was no statistically difference in subjective score of image quality between the two sequences.SNR and CNR of the ACS 3D-FLAIR sequence were significantly higher than those of the uCS 3D-FLAIR sequence(P<0.001).The kappa values of grades of cochlear and vestibular endolymphatic hydrops were 0.942 and 0.888 using two sequences(P<0.001).The kappa values of grades of cochlear and vestibular endolymphatic hydrops using the ACS 3D-FLAIR sequence between the two doctors were 0.784 and 0.831,respectively(P<0.001);the kappa values of grades of cochlear and vestibular endolymphatic hydrops using uCS 3D-FLAIR sequence between the two doctors were 0.725 and 0.756,respectively(P<0.001).Conclusions ACS 3D-FLAIR could provide higher SNR and CNR than uCS 3D-FLAIR,and is more suitable for intravenous gadolinium contrast-enhanced magnetic resonance imaging of the inner ear;the endolymphatic hydrops grades using ACS 3D-FLAIR is similar to use uCS 3D-FLAIR.

ObjectiveTo evaluate the value of an optimized three-dimensional inversion-recovery with real reconstruction (3D-real IR) sequence with a longer repetition time (TR, 16 000 ms) based on modulated flip angle technique in refocused imaging with extended echo train (MATRIX) in the endolymphatic hydrops (EH) imaging after intratympanic gadolinium (Gd) administration, and to compare it with a conventional 3D-real IR based on the turbo spin echo (TSE) sequence. MethodsFrom July 2021 to November 2022, twenty-seven patients received both the conventional and optimized 3D-real IR sequences after bilateral intratympanic Gd administration. Images of the two sequences were qualitativly evaluated and compared. Contrast-to-noise ratio (CNR), signal-to-noise ratio (SNR), and area ratio of endolymph against the total lymphatic space from the two sequences were measured and compared. Results14(25.9%) ears with insufficient contrast for the EH diagnosis on the conventional sequence were clearly displayed on the optimized sequence. Image score, CNR and SNR of the optimized sequence were significantly higher than those of the conventional sequence (P ＜ 0.001). The scanning time of two sequences was similar. The area ratio of endolymph against the total lymphatic space in the cochlear was significantly higher on the conventional 3D-real IR than that on the optimized 3D-real IR (P ＜ 0.001); there was no statistical difference in the vestibule between the two sequences. ConclusionsCompared with conventional sequence, optimized 3D-real IR sequence with a longer TR may be better for evaluation of EH after intratympanic Gd administration.

BACKGROUND:Ménière's disease (MD) remains a heterogeneous disorder with unclear pathogenesis. While immune dysregulation has been implicated, the specific role of CD4+ T cell subsets and their clinical correlations in MD are poorly understood. METHODS:We performed comprehensive immune profiling of 30 MD patients and 27 healthy controls using flow cytometry to analyze six CD4+ T cell subsets (Th1, Th2, Th17, Treg, TGF-β+, TNF-α+) and multiplex cytokine analysis of 16 inflammatory mediators plus IgE. Unsupervised hierarchical clustering identified distinct immune phenotypes, and cox regression analysis determined biomarkers of disease activity. RESULTS:Three distinct immunophenotypes were identified: Autoinflammatory (35.7 %, elevated Th1/TNF-α + cells), inactive (28.6 %, balanced profiles), and type 2-skewed (35.7 %, increased Treg/TGF-β + cells). MD patients showed significantly altered Th1/Th2/Th17 balance with elevated TGF-β + cells (p < 0.001) and decreased serum IFN-γ, IL-1β, and IL-17 a levels, while CCL3/CCL4 chemokines were increased. Cluster-specific immune-clinical correlations revealed distinct pathophysiological patterns. IL-2Rα (HR = 0.18, p = 0.007) and IFN-γ (HR = 0.26, p = 0.046) may represent biomarkers of disease activity. CONCLUSION:MD exhibits significant immunological heterogeneity with three distinct CD4+ T cell-defined phenotypes. These findings support the development of personalized treatment approaches and suggest potential biomarkers of disease activity, advancing our understanding of MD pathogenesis through comprehensive immune profiling.

In ophthalmology, the quality of fundus images is critical for accurate diagnosis, both in clinical practice and in artificial intelligence (AI)-assisted diagnostics. Despite the broad view provided by ultrawide-field (UWF) imaging, pseudocolor images may conceal critical lesions necessary for precise diagnosis. To address this, we introduce UWF-Net, a sophisticated image enhancement algorithm that takes disease characteristics into consideration. Using the Fudan University Ultra-wide-field Image (FDUWI) dataset, which includes 11 294 Optos pseudocolor and 2 415 Zeiss true-color UWF images, each of which is rigorously annotated, UWF-Net combines global style modeling with feature-level lesion enhancement. Pathological consistency loss is also applied to maintain fundus feature integrity, significantly improving image quality. Quantitative and qualitative evaluations demonstrated that UWF-Net outperforms existing methods such as contrast limited adaptive histogram equalization (CLAHE) and structure and illumination constrained generative adversarial network (StillGAN), delivering superior retinal image quality, higher quality scores, and preserved feature details after enhancement. In disease classification tasks, images enhanced by UWF-Net showed notable improvements when processed with existing classification systems over those enhanced by StillGAN, demonstrating a 4.62% increase in sensitivity (SEN) and a 3.97% increase in accuracy (ACC). In a multicenter clinical setting, UWF-Net-enhanced images were preferred by ophthalmologic technicians and doctors, and yielded a significant reduction in diagnostic time ((13.17 ± 8.40) s for UWF-Net enhanced images vs (19.54 ± 12.40) s for original images) and an increase in diagnostic accuracy (87.71% for UWF-Net enhanced images vs 80.40% for original images). Our research verifies that UWF-Net markedly improves the quality of UWF imaging, facilitating better clinical outcomes and more reliable AI-assisted disease classification. The clinical integration of UWF-Net holds great promise for enhancing diagnostic processes and patient care in ophthalmology.

Context Hereditary distal renal tubular acidosis caused by SLC4A1 gene mutation (SLC4A1-dRTA) is a rare hereditary form of renal tubular acidosis. Rickets or osteomalacia is a common complication of SLC4A1-dRTA and seriously affects patients' daily lives. However, studies on the bone microstructure in SLC4A1-dRTA are limited.Objective This work aimed to evaluate the bone microstructure of SLC4A1-dRTA patients, compared to age- and sex-matched healthy controls and X-linked hypophosphatemic rickets (XLH) patients.Methods This was a retrospective study of 11 SLC4A1-dRTA patients. Clinical manifestations and biochemical and radiographical examinations were characterized. Bone microstructure was examined in 7 SLC4A1-dRTA patients, 7 healthy controls, and 21 XLH patients using high-resolution peripheral quantitative computed tomography.Results Skeletal symptoms, including fracture, bone pain, and lower limb deformity, were present in 72.7% of SLC4A1-dRTA patients. Short stature was present in 63.6% of the patients. SLC4A1-dRTA patients had significantly lower volumetric bone mineral density in the distal tibia and more severe deteriorated trabecular bone in the distal radius and tibia than healthy controls. SLC4A1-dRTA patients had significantly more severely deteriorated trabecular bone in the distal radius and distal tibia compared to XLH patients. With long-term alkaline therapy, SLC4A1-dRTA patients had alleviated bone pain and increased height.Conclusion Skeletal lesions were common clinical manifestations in SLC4A1-dRTA patients. Compared with XLH, another common type of rickets, SLC4A1-dRTA patients had more severe trabecular bone microstructure damage, further supporting the necessity of early diagnosis and timely treatment of the disease.

ObjectiveThis study revealed a core regulator and common upstream mechanisms for the multifaceted pathological processes of age-related macular degeneration (AMD) and provided proof-of-concept for this new therapeutic target.MethodsComprehensive gene expression analysis was performed using RNA sequencing of eye cup from old mice as well as laser-induced choroidal neovascularization (CNV) mouse model. Through integrative analysis and protein-protein interaction (PPI) analysis, common pathways and key transcription factor was identified simultaneously engaged in age-related retinal degeneration and CNV, the two typical pathological process of AMD. Subsequently, the expression changes of Spi1, the key regulator, as well as the alternation of the downstream mechanisms were validated in both models through qRT-PCR, Elisa, flow cytometry and immunofluorescence. Further, we assessed the impact of Spi1 knockdown in vitro and in vivo using gene intervention vectors carried by adeno-associated virus or lentivirus to test its potential as a therapeutic target.ResultsCompared to corresponding controls, we found 1,939 and 1,319 genes differentially expressed in eye cups of old and CNV mice respectively. The integrative analysis identified a total of 275 overlapping DEGs, of which 150 genes were co-upregulated. PPI analysis verified a central transcription factor, SPI1. The significant upregulation of Spi1 expression was then validated in both models, accompanied by macrophage polarization towards the M1 phenotype. Finally, SPI1 suppression significantly inhibited M1 polarization of BMDMs and attenuated neovascularization in CNV mice.ConclusionThis study demonstrates that SPI1 exerts a pivotal role in AMD by regulation of macrophage polarization and innate immune response, offering promise as an innovative target for treating AMD.

Rationale: Angiogenesis expedites tissue impairment in many diseases, including age-related macular degeneration (AMD), a leading cause of irreversible blindness in elderly.A substantial proportion of neovascular AMD patients, characterized by aberrant choroidal neovascularization (CNV), exhibit poor responses or adverse reactions to anti-VEGF therapy.Herein, we aimed to unveil the function of newly identified transfer RNA-derived small RNA, tRF-Glu-CTC, in the pathology of CNV and determine its potential in inhibiting angiogenesis.Methods: Small non-coding RNA sequencing and quantitative polymerase chain reaction were conducted to detect expression pattern of tRF-Glu-CTC in CNV development.Immunofluorescence staining, fundus fluorescein angiography and ex vivo choroidal sprouting assays were employed for the evaluation of tRF-Glu-CTC's function in CNV development.The role of tRF-Glu-CTC in endothelial cells were determined by in vitro endothelial cell proliferation, migration and tube formation assays.Transcriptome sequencing, dual-luciferase reporter assay and in vitro experiments were conducted to investigate downstream mechanism of tRF-Glu-CTC mediated pathology.Results: tRF-Glu-CTC exhibited substantial up-regulation in AMD patients, laser-induced CNV model, and endothelial cells under hypoxia condition, which is a hallmark of CNV.Inhibiting tRF-Glu-CTC reduced angiogenesis and hypoxia stress in the neovascular region without neuroretina toxicity in laser-induced CNV model, showing an anti-angiogenic effect comparable to bevacizumab, while overexpression of tRF-Glu-CTC significantly augmented CNV.Mechanically, under hypoxia condition, angiogenin was involved in the production of tRF-Glu-CTC, which in turn triggered endothelial cell tubulogenesis, migration and promoted the secretion of inflammatory factors via the suppression of vasohibin 1 (VASH1).When downregulating VASH1 expression, the inhibition of tRF-Glu-CTC showed minimal suppression on angiogenesis.Conclusions: This study demonstrated the important role of tRF-Glu-CTC in the progression of angiogenesis.Targeting of tRF-Glu-CTC may be an alternative to current anti-VEGF therapy for CNV in AMD and other conditions with angiogenesis.

Abstract Intensive medical management has been recommended to ischemic stroke of intracranial atherosclerosis (ICAS), but 9.4–15% probability of recurrent stroke remains an inevitable reality. The characteristics of high-risk intracranial plaque that contribute to stroke recurrence after intensive therapy is unclear. The patients of acute ischemic stroke due to ICAS from two centers were prospectively analyzed, who underwent the 3D head&neck high-resolution vessel wall magnetic resonance imaging (hr-VW-MRI) at baseline and received intensive medical management within 90 days. The morphological features, such as minimal lumen area (MLA), and histogram parameters including entropy were assessed based on hr-VW-MR images. The recurrence of ischemic events after 6 months was defined as hyperintensity on diffusion-weighted images in the ipsilateral vascular territory. 222 patients (age, 59.5 ± 12.1; males, 153) were finally included, and 38 have recurrent stroke after 6 months. After adjusting the age and gender, Cox regression demonstrated that smoking (HR = 4.321; 95%CI, 1.838–10.161; P = 0.001), taking exercise (HR = 0.409; 95%CI, 0.198–0.843; P = 0.015), blood pressure management (HR = 0.180; 95%CI, 0.073–0.443; P = 0.001), MLA (HR = 0.771; 95%CI, 0.625–0.951; P = 0.015) and entropy (HR = 0.274; 95%CI, 0.130–0.576; P = 0.001) were significant predictors of recurrent ischemic stroke. However, the area under curve value of MRI parameters was significantly higher than that of traditional clinical factors (0.859 vs 0.789; P = 0.01). The plaque characteristics based on hr-VW-MRI may provide complementary values over traditional clinical features in predicting ischemic recurrence for ICAS.

AimTo investigate the molecular mechanism underlying the onset of choroidal neovascularization (CNV).MethodsIntegrated transcriptomic and proteomic analyses of retinas in mice with laser-induced CNV were performed using RNA sequencing and tandem mass tag. In addition, the laser-treated mice received systemic interferon-β (IFN-β) therapy. Measurements of CNV lesions were acquired by the confocal analysis of stained choroidal flat mounts. The proportions of T helper 17 (Th17) cells were determined by flow cytometric analysis.ResultsA total of differentially expressed 186 genes (120 up-regulated and 66 down-regulated) and 104 proteins (73 up-regulated and 31 down-regulated) were identified. The gene ontology and KEGG pathway analyses indicated that CNV was mainly associated with immune and inflammatory responses, such as cellular response to IFN-β and Th17 cell differentiation. Moreover, the key nodes of the protein–protein interaction network mainly involved up-regulated proteins, including alpha A crystallin and fibroblast growth factor 2, and were verified by Western blotting. To confirm the changes in gene expression, real-time quantitative PCR was performed. Furthermore, levels of IFN-β in both the retina and plasma, as measured by enzyme-linked immunosorbent assay (ELISA), were significantly lower in the CNV group than in the control group. IFN-β treatment significantly reduced CNV lesion size and promoted the proliferation of Th17 cells in laser-treated mice.ConclusionsThis study demonstrates that the occurrence of CNV might be associated with the dysfunction of immune and inflammatory processes and that IFN-β could serve as a potential therapeutic target.

Biochar (BC) is a stable, carbon-rich material produced through biomass pyrolysis in an oxygen-restricted environment. In recent years, BC has gained recognition as an environmentally friendly material and has been extensively researched for its various applications related to human health. However, the medical applications of biochar remain relatively unexplored. This review aims to analyze recent publications from PubMed, focusing on the direct association between biochar and medical science over the past 3 years. The analysis identified five main subjects: contaminant immobilization, medical waste treatment and nutrient recovery, biochar toxicity, electrical sensors and biosensors, and drug delivery. Among these subjects, drug delivery and biosensors demonstrated the most direct relevance to the medical field. To enhance the validity of our findings, a bibliometric analysis was performed using the Web of Science Core Collection to visualize the trends in medical applications of biochar over time. The results further support our analysis. Finally, potential directions for future medical applications of biochar were discussed. This review underscores the necessity for further research on the medical applications of biochar. By exploring its potential in drug delivery, biosensors, and other domains, biochar has the potential to revolutionize medicine. Graphical Abstract