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The role of endoscopic therapies for patients with metabolic dysfunction-associated steatotic liver disease (MASLD).
Expert Rev Gastroenterol Hepatol
Joan Llach, Anna Soria, Isabel Graupera +1 more
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a major public health challenge closely linked to obesity and metabolic syndrome. Effective, durable weight-loss strategies are needed to modify its natural history, particularly in patients at high surgical risk or with limited response to pharmacotherapy.
Development of bacterial cellulose-based polymeric cryogel scaffold as an eco-friendly biomaterial.
Colloids Surf B Biointerfaces
Hao An, Hyun-Woo Choi, Yong-Seok Jang +2 more
Cryogels with interconnected macroporous structures are promising three-dimensional scaffolds that facilitate cell infiltration, nutrient transport, and tissue development. This study compared two cryogel systems: gelatin methacryloyl cryogels prepared by free-radical polymerization and oxidized bacterial cellulose-gelatin cryogels synthesized through a green, initiator-free Schiff-base crosslinking method. Both scaffolds exhibited favorable elasticity and biocompatibility, but oxidized bacterial cellulose-gelatin cryogels maintained stable pore structures upon rehydration and showed superior mechanical integrity due to the nanofibrous cellulose framework. Murine preosteoblasts cultured on oxidized bacterial cellulose-gelatin scaffolds exhibited enhanced proliferation and osteogenic differentiation, attributed to optimal pore size and the absence of cytotoxic crosslinking residues. Furthermore, Bovine muscle satellite cells exhibited better spreading and a denser PAX7-positive distribution on oxidized bacterial cellulose-gelatin cryogels, suggesting that the stable porous architecture may support satellite cell maintenance and expansion. These findings demonstrate that tuning pore architecture and using biocompatible crosslinking chemistry significantly improve cryogel scaffold performance. The oxidized bacterial cellulose-gelatin cryogel presents a promising, versatile platform for both hard and soft tissue engineering applications.
Effect of supplemental hydrocortisone during stress in prednisolone-induced adrenal insufficiency: a study protocol for a multicentre, randomised, double-blinded, placebo-controlled clinical trial on health-related quality of life in patients with polymyalgia rheumatica/giant cell arteritis on low-dose prednisolone treatment (the RESCUE study).
BMJ Open
Stina Willemoes Borresen, Simon Bøggild Hansen, Hajir Al-Jorani +15 more
Patients on low-dose prednisolone may develop adrenal insufficiency causing reduced health-related quality of life (HRQoL) and increased risk of adrenal crisis. This study examines whether supplemental hydrocortisone during mild to moderate stress improves HRQoL in patients with polymyalgia rheumatica/giant cell arteritis (PMR/GCA) with adrenal insufficiency on low-dose prednisolone.
A unimolecular GLP-1 and FGF21 dual agonist for treatment of metabolic dysfunction-associated steatohepatitis.
Commun Med (Lond)
Parul Sirohi, Seh-Hoon Oh, Catherine G Price +7 more
Metabolic dysfunction-associated steatohepatitis is a progressive liver disease characterized by inflammation and fibrosis, for which effective pharmacological treatments remain limited. Hormones that regulate metabolism, such as glucagon-like peptide-1 and fibroblast growth factor-21, have shown therapeutic promise through complementary metabolic and hepatoprotective actions. This study aims to develop and evaluate a single molecular therapy that engages both pathways to address multiple drivers of disease progression.
LncRNA TUG1 promotes hypertrophic scar formation via the miR-627/IGF1R axis.
J Mol Histol
Zeming Bai, Ziyang Han, Xiangzi Kong +7 more
Hypertrophic scars (HS) are fibrotic skin disorders driven by abnormal fibroblast activity. The molecular mechanisms underlying HS remain incompletely understood, particularly the role of non-coding RNAs. Expression levels of lncRNA TUG1, miR-627, and IGF1R were measured in HS tissues and fibroblasts using qRT-PCR and Western blotting. Dual-luciferase assays validated direct interactions. Functional effects of TUG1 and miR-627 on fibroblast proliferation and migration were assessed using MTT and Transwell assays. A rabbit ear model of HS was used to examine in vivo effects of TUG1 and miR-627 modulation on scar formation and molecular expression. TUG1 was significantly upregulated in HS tissues and inversely correlated with miR-627, which was downregulated. TUG1 promoted fibroblast proliferation and migration by directly sponging miR-627, thereby lifting repression on IGF1R, a known pro-fibrotic effector. Luciferase assays confirmed direct binding of miR-627 to both TUG1 and IGF1R. Co-transfection of miR-627 attenuated TUG1-induced IGF1R upregulation and reversed its pro-fibrotic cellular effects. In vivo, TUG1 overexpression led to increased scar thickness, collagen deposition, and IGF1R expression, while miR-627 overexpression mitigated these effects. Co-administration of both restored scar morphology and molecular markers to near-control levels. TUG1 promotes hypertrophic scar formation by sponging miR-627 and derepressing IGF1R. This newly identified TUG1-miR-627-IGF1R axis plays a central role in HS pathogenesis and may serve as a promising therapeutic target for fibrotic skin disease.
Serum from Fibromyalgia Patients Activates Satellite Glial Cells in Mouse Peripheral Ganglia.
Cells
Menachem Hanani, Rachel Feldman-Goriachnik, Suhail Aamar
Fibromyalgia (FM) is a complex syndrome associated with chronic widespread pain and with various other symptoms, including sleep and mood disturbances. Its underlying causes are not fully understood, and the lack of diagnostic blood tests and imaging, along with the absence of definitive treatments, makes management challenging. Recent studies showed that passive transfer of immunoglobulins from FM patients into mice activated satellite glial cells (SGCs) in mouse dorsal root ganglia (DRG), leading to pain behaviors. Here, we aimed to determine whether whole serum from FM patients activates mouse SGCs in DRGs and other ganglia that may be involved in FM's diverse symptoms. Serum from FM patients (N = 15) and healthy controls (HCs, N = 8) was collected. Sera were incubated with different types of mouse sensory ganglia: DRG, trigeminal ganglion (TG), the nodose ganglion (NG), and the superior cervical sympathetic ganglion (Sup-CG). SGC activation was assessed by immunostaining of SGCs for the glial activation marker glial fibrillary acidic protein (GFAP). All the ganglia tested, DRG, TG, NG, and Sup-CG, displayed induced upregulation of GFAP labeling in SGCs after incubation with FM serum compared with HCs, indicating SGC activation by the serum. Similar responses were observed in both male and female mice. We conclude that serum from FM patients contains factors that can activate SGCs across various types of mouse ganglia, which may reflect the diverse symptom profile of FM. These findings provide evidence for pathogenic factors that could serve as a foundation for a diagnostic method for FM and require further purification and identification, hopefully paving the way for future targeted FM therapy.
The Role of Leukemia Inhibitory Factor in Attenuating Skeletal Muscle Atrophy: Mechanisms to Exercise Interventions.
Cells
Na Jiang, Shiyi Wang, Jiaqiao Zhang +1 more
Leukemia inhibitory factor (LIF), a member of the interleukin-6 (IL-6) cytokine family, is a well-characterized myokine with pleiotropic regulatory effects on skeletal muscle. LIF modulates several fundamental cellular processes, including myoblast proliferation, apoptosis, angiogenesis, and energy metabolism. Exercise upregulates LIF expression in skeletal muscle, thereby promoting satellite cell activation, proliferation, myoblast differentiation, and angiogenesis, facilitating physiological muscle hypertrophy, and suppressing myocyte apoptosis and muscle atrophy. In addition, LIF plays a critical role in modulating the inflammatory and extracellular matrix remodeling following exercise-induced muscle damage, thereby supporting efficient muscle repair and regeneration. This review elaborates on the biological mechanisms by which LIF regulates skeletal muscle atrophy and contributes to the enhancement of skeletal muscle function. It also highlights the biological characteristics of myogenic LIF and discusses future directions for basic and applied research on exercise interventions targeting LIF signaling pathways.
Single-Cell RNA Sequencing Reveals Cellular Heterogeneity and Developmental Dynamics of Goose Satellite Cells During Embryogenesis.
Cells
Cui Wang, Yi Liu, Guitao Jiang +5 more
Skeletal muscle satellite cells (SMSCs) are essential for embryonic myogenesis and postnatal muscle regeneration; however, their cellular heterogeneity and transcriptional dynamics during avian development remain largely unexplored. Here, we performed single-cell RNA sequencing (scRNA-seq) on 42,886 cells isolated from goose leg muscles across four embryonic stages (E13, E15, E18, and E23), with each stage comprising pooled tissues from four female embryos. Unbiased clustering resolved 22 transcriptionally distinct clusters representing six major cell types-satellite cells, myocytes, fibro-adipogenic progenitors, endothelial cells, immune cells, and Schwann cells-with satellite cells being the most abundant. Satellite cells were further subdivided into three functional states (quiescent, activated, and proliferative/differentiating), which followed a continuous, linear pseudotime trajectory from early to late embryonic stages. This trajectory was marked by a progressive downregulation of stemness-associated regulators (e.g., PAX7) and upregulation of myogenic commitment and differentiation factors (e.g., MYF5, MYOD1, and MYOG), faithfully mirroring chronological development. Cell-cell communication analysis revealed that quiescent satellite cells exhibited the most extensive intercellular signaling networks (e.g., FGFR, Ephrin, collagen, CADM), whereas activated and proliferative/differentiating cells showed progressively diminished communication capacity. Across developmental stages, the contribution intensities of key signaling pathways-including SEMA6, CDH, FGF, LAMININ, MK, MPZ, CADM, FN1, and COLLAGEN-varied significantly among satellite cell states, indicating state-specific responsiveness to microenvironmental cues. Collectively, these findings demonstrate that satellite cells dynamically coordinate extrinsic signal integration with intrinsic differentiation programs to achieve orderly myogenic progression. This study provides a high-resolution single-cell atlas of goose SMSC development, uncovering subpopulation heterogeneity, state-specific molecular signatures, and key signaling pathways, with important implications for avian muscle biology and genetic improvement of poultry.
Efficacy and Safety of Oral Semaglutide in the Management of Diabetes and Obesity: A Comprehensive Meta-analysis of Real-world Evidence.
touchREV Endocrinol
Sweekruti Jena, Radhika Jindal, Deep Dutta +2 more
Oral semaglutide is the only oral glucagon-like peptide-1 receptor agonist approved for type 2 diabetes (T2D) management. Although its efficacy and safety are established from randomized controlled trials (RCTs), real-world evidence (RWE) may differ. No comprehensive systematic review and meta-analysis (SRM) has holistically analysed the RWE on oral semaglutide. This SRM analysed the RWE outcomes of oral semaglutide.
Towards Sustainable Synthesis of Peptide Therapeutics via Tag-Assisted Peptide Synthesis and Aryl Selenoester Aminolysis Ligation.
J Am Chem Soc
Peter H G Egelund, Ayman Rachid, Anthony Ayoub +7 more
There has been a recent renaissance in the use of peptides as therapeutic agents across a range of indications, sparking significant demand for the development of sustainable and cost-effective alternatives to solid-phase peptide synthesis (SPPS) for the production of these molecules, particularly in the pharmaceutical industry. While tag-assisted peptide synthesis (TAPS) has offered promise, this methodology cannot be routinely used to assemble longer peptide targets (>20 residues), limiting its utility for most peptide therapeutics. Fragment condensation of side-chain-protected peptides using coupling reagents is typically used to prepare larger targets, but this approach usually leads to unacceptable levels of epimerization without significant optimization. Herein, we report an efficient platform for the synthesis of pharmaceutically relevant peptides through direct aminolysis of peptide aryl selenoesters generated via TAPS. Notably, this novel ligation method circumvents the limitations of peptide length associated with TAPS, leads to minimal epimerization, and significantly reduces reagent and solvent use, making it attractive from an environmental standpoint. By integrating the aryl selenoester aminolysis ligation (ASAL) into the TAPS workflow, the convergent synthesis of several therapeutic peptides of increasing complexity was successfully accomplished, including osteoporosis drug teriparatide (34 residues), sulfated tsetse fly-derived thrombin-inhibiting anticoagulant TTI (32 residues), and tirzepatide (39 residues), used for the treatment of type 2 diabetes and weight management. When used in concert with TAPS, the ASAL reaction developed here can serve as a robust method for the ligation-based assembly of tagged peptides, creating a scalable route to access peptide-based therapeutics across academia and industry with a low environmental impact.
Honokiol-loaded nanomicelles reprogram senescence and immune evasion in hepatocellular carcinoma via SIRT3-mediated mitochondrial stabilization.
Bioeng Transl Med
Wenxing Deng, Yizhi Wu, Yisheng Yin +1 more
Hepatocellular carcinoma (HCC) is a major cause of cancer-related deaths. Advanced-stage patients face poor prognosis due to chemotherapy resistance and an immunosuppressive tumor microenvironment (TME). Cellular senescence, marked by the senescence-associated secretory phenotype, promotes tumor progression and immune evasion. Although honokiol (HKL) shows strong antitumor activity, its clinical use is limited by poor solubility, rapid clearance, and low bioavailability. Here, we report HKL-loaded poly(ethylene glycol)-poly(ε-caprolactone)-poly(ethylene glycol) triblock copolymer nanomicelles (HKL-nm) as a multifunctional nanotherapeutic platform. HKL-nm exhibited a uniform spherical shape with a diameter of 60.93 ± 5.7 nm, near-neutral charge (-0.28 ± 0.1 mV), and high encapsulation efficiency (85.9 ± 4.9%). It enabled sustained drug release (70.04 ± 6.2% over 200 h) and significantly improved oral pharmacokinetics (area under the curve increased 6.26-fold and C max increased 4.06-fold). Specifically, the HKL drug concentration at the tumor site was enhanced by 3.52-fold. Mechanistically, HKL-nm suppressed senescence markers (p53, p16, and p21) and senescence-associated β-galactosidase positivity via a Sirtuin 3-dependent pathway, inhibiting cytoplasmic mitochondrial DNA leakage and cGAS-STING signaling. In Hepa1-6 cells xenografts, combination therapy with HKL-nm and the senolytic cocktail dasatinib + quercetin achieved tumor volume reduction, with transcriptomic analysis validating enrichment of immune activation pathways. This was accompanied by enhanced infiltration of CD8+ cytotoxic T cells and mature dendritic cells, coupled with profound suppression of myeloid-derived suppressor cells. By integrating nanodelivery, senescence modulation, and immuno-oncology, HKL-nm represents a promising strategy to overcome therapeutic resistance in HCC, providing a preclinical basis for translation to solid tumors.
Long-Distance Trail Running Induces Inflammatory-Associated Protein, Lipid, and Purine Oxidation in Red Blood Cells.
Blood Red Cells Iron
Travis Nemkov, Emeric Stauffer, Francesca Cendali +10 more
Ultra-endurance running imposes extreme demands on oxygen transport, yet how red blood cells (RBCs) respond at the molecular level remains poorly defined. We integrated plasma and RBC multi-omics with hematology and hemorheology in athletes sampled before and after two trail races of distinct duration: a 40-km marathon (MCC) and a 171-km ultramarathon (UTMB). Both races elicited systemic inflammation, but UTMB was distinguished by marked IL-6 and kynurenine increases, acute-phase protein induction, and profound lipid remodeling. In RBCs, acylcarnitine accumulation, pantothenate depletion, and oxidized lipid species indicated Lands cycle activation, while purine salvage and carboxylate metabolism reflected redox-sensitive rerouting of energy pathways. Proteomics revealed non-random oxidation, particularly methionine oxidation of antioxidant enzymes, metabolic proteins, and proteasome components, correlating with impaired deformability as gleaned by testing of rheological properties. Elevated copper provided an additional correlate of reduced RBC mechanics. Despite minimal signatures of intravascular hemolysis, plasma bilirubin and hypoxanthine rose, consistent with extravascular clearance of damaged RBCs. Collectively, these results demonstrate that ultra-running accelerates RBC aging through inflammatory and oxidative pathways beyond mechanical trauma, linking systemic cytokine responses to molecular lesions, biomechanical dysfunction, and splenic sequestration. These findings not only identify actionable biomarkers of exercise-induced hemolysis but also provide translational insight into oxidative lesions that similarly limit RBC survival in transfusion and inflammatory disease settings.
Bridging aging and colorectal cancer: synergistic roles of inflammaging and immunosenescence.
Front Immunol
Silvere D Zaongo, Qiyu Yang, Mei Han +5 more
Colorectal cancer (CRC) is one of the most commonly occurring malignancies worldwide, with incidence and mortality rising sharply in older adults. While aging is increasingly recognized as a key risk factor for CRC, the fundamental immunological mechanisms which underlie this risk remain incompletely understood. Two interconnected processes, namely inflammaging and immunosenescence, appear central to this association. On the one hand, inflammaging, which is characterized by chronic low-grade inflammation in older individuals, fosters a tumor-promoting microenvironment through oxidative stress, genomic instability, and persistent cytokine activation. On the other hand, immunosenescence diminishes immune surveillance, reducing the clearance of premalignant cells and weakening responses to tumor progression and therapy. Together, these processes create an immunological framework that predisposes the aging colon to malignant transformation. This review synthesizes current knowledge of the cellular and mechanistic impacts of inflammaging and immunosenescence in CRC pathogenesis, highlighting their roles in shaping disease susceptibility in the elderly. These insights may guide future endeavor in biomarker discovery, prevention, and therapeutic intervention to mitigate the burden of CRC in aging populations.
Mechanisms by Which Exercise Delays Brain Aging Through Regulation of the Mitochondrial Quality Control System.
Biology (Basel)
Xinyi Zhu, Lei Shi, Yahong Dong +2 more
Brain aging is a complex biological process characterised by progressive neuronal and synaptic decline, in which disruption of mitochondrial quality control plays a central role. This system encompasses multiple synergistic components, including mitochondrial biogenesis, dynamic equilibrium, autophagic clearance, and energy metabolism. Aging induces dysfunction across these processes, precipitating mitochondrial fragmentation, functional decline, and energy crises, ultimately driving cognitive deterioration. Exercise is a promising non-pharmacological intervention for preserving brain health during aging, and its benefits may be mediated, at least in part, through modulation of mitochondrial quality control. Specifically, exercise has been shown to activate key signaling pathways such as AMPK/SIRT1/PGC-1α, thereby promoting mitochondrial biogenesis and metabolic adaptation. It may also regulate mitochondrial dynamics and mitophagy via pathways including cAMP/PKA/Drp1 and AMPK/mTOR. In addition, emerging evidence indicates that exercise may influence brain mitochondrial function through activity-dependent regulation of mitochondrial gene expression and systemic signaling factors. Furthermore, this review discusses potential differences between exercise modalities and highlights future directions for personalised intervention strategies, providing a theoretical basis for the application of exercise in delaying brain aging and preventing neurodegenerative diseases.
Network pharmacology and experimental evaluation of Sanwei Tanxiang Tangsan in doxorubicin-induced heart failure.
J Cardiothorac Surg
Davaadagva Aruna, Battulga Dulan, Hua Damdinjav +3 more
Heart failure (HF) is a complex syndrome characterized by inflammation, oxidative stress, and cardiomyocyte apoptosis, for which effective and well-tolerated therapies remain limited. This study sought to explore the potential mechanisms by which Mongolian medicine Sanwei Tanxiang Tangsan (STX) may be associated with AKT1/p53-related signaling in the mitigation of HF, employing network pharmacology, molecular docking, and animal experimentation.
Extreme Heterophilic Antibody Interference in BNP Immunoassay: A Case Report and Systematic Investigation Protocol.
J Clin Lab Anal
Huicong Yang, Yuanhai Zheng, Zhenhua Zeng +4 more
Heterophilic antibody (HA) interference remains a persistent challenge in immunoassay diagnostics. Human anti-mouse antibodies (HAMA) can cause spuriously elevated biomarker results, potentially leading to misdiagnosis and unnecessary clinical interventions. Brain natriuretic peptide (BNP) is critical for heart failure diagnosis, but false-positive results due to HAMA may trigger inappropriate clinical management.
Neuroendocrine Regulation of Female Fertility: The Role of CNS-Derived Hormones.
J Mol Endocrinol
Amirreza Shakoeizadeh, Erfan Shahabinejad, Mahdi Heydari +2 more
Infertility is an increasing concern for many women and can affect both physical and emotional well-being. The central nervous system (CNS) -particularly the hypothalamus, pituitary gland, and pineal gland - plays a crucial role in female reproductive health. We conducted a narrative review of relevant studies published between 2015 and 2025, sourcing data from PubMed and Scopus. Our goal was to investigate how dysregulation of hormones from the hypothalamus, pituitary gland, and pineal gland contributes to fertility-related disorders, such as impairments in ovulation, oocyte quality, and embryo development. Both human and significant animal studies were considered to better understand how CNS hormones affect fertility. The findings emphasize the roles of key hormones, including gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), melatonin, Adrenocorticotropic Hormone (ACTH), Thyroid-Stimulating Hormone (TSH), and vasopressin (ADH). The proper timing and balance of these hormones are vital. For instance, GnRH pulses regulate the release of LH and FSH, which are essential for ovulation and follicle development. Melatonin supports oocyte health and helps maintain the menstrual cycle, while ACTH and TSH are also involved in reproductive function. Vasopressin contributes by affecting uterine activity and hormone production. Understanding these hormonal interactions may lead to better diagnostic tools and more effective treatment strategies for conditions such as polycystic ovary syndrome (PCOS) and other fertility-related disorders. Unlike previous studies, this research provides a comprehensive investigation of how CNS-mediated hormonal regulation influences female reproductive outcomes, examining the roles of all involved hormones.
Alternating Therapy With Osilodrostat and Etomidate in Severe Ectopic Cushing's Syndrome Complicated by Silent Bowel Perforation.
Case Rep Endocrinol
Hery Mejia, Carmen Villabona, Renato Savian +7 more
Ectopic adrenocorticotropic hormone (ACTH)-dependent Cushing's syndrome (CS), ectopic ACTH secretion (EAS) is a rare condition caused by ACTH-secreting neuroendocrine tumors (NETs), such as bronchial carcinoids. We report a 65-year-old woman with severe EAS complicated by bowel perforation. She presented with hypokalemia (K+ 2.3 mmol/L), metabolic alkalosis, resistant hypertension (180/110 mmHg), worsening diabetes (HbA1c 6.7%-9.1%), proximal muscle weakness, and 14 kg weight gain over 3 months. A silent sigmoid colon perforation required emergency resection and colostomy. Biochemical tests confirmed hypercortisolism (urine free cortisol [UFC], 1256 µg/24 h, plasma ACTH 175 pg/mL, and cortisol >40 µg/dL post-dexamethasone). Imaging identified a 2.3 cm pulmonary nodule with mild uptake on Ga-68 DOTATATE PET/CT. Bronchoscopic biopsy confirmed an ACTH-positive low-grade bronchial carcinoid tumor. Initial treatment with osilodrostat was interrupted due to acute illness and oral medication intolerance. Intravenous etomidate was employed in the ICU for rapid cortisol suppression, followed by resumption of osilodrostat after stabilization. Thoracoscopic lobectomy confirmed a low-grade carcinoid tumor (Ki-67 < 2%). Postoperatively, cortisol normalized, electrolytes stabilized, and HbA1c improved to 6.5%. This case highlights bowel perforation as a severe complication of EAS and underscores the importance of dynamic, alternating therapy with osilodrostat and etomidate, along with individualized surgical and medical management strategies.
The Role of High-Protein Instant Ramen Noodles in Inducing and Maintaining Satiety: Acute, Randomized, Crossover Study.
Nutr Diabetes
Princess U Ozioma, Gaurav M Kudchadkar, Sara Ranjbar +6 more
This study tested if a breakfast meal of high-protein instant ramen noodles would increase satiety, reduce hunger, improve glycemic response, and reduce lunch-time energy intake compared to an isocaloric breakfast of standard protein instant ramen noodles.
Magnetic enrichment and enabled cascade amplification for ultrasensitive SPR analysis of PD-L1+ exosomes.
Biosens Bioelectron
Hezhen Liu, Zhaofei Liu, Kwangnak Koh +1 more
Exosomes serve as stable liquid-biopsy biomarkers for early cancer detection due to their molecular resemblance to parent cells. Here, a magnetic enrichment-assisted surface plasmon resonance (SPR) assay is developed based on Zr/Ce-MOF@Fe3O4 core-satellite nanocomposites for sensitive exosome analysis. The Zr/Ce-MOF is constructed with Zr as the metal node and doped with Ce, exhibiting intrinsic oxidase-like activity through the Ce3+/Ce4+ redox cycle. It catalyzes the oxidation of 3,3',5,5'-tetramethylbenzidine without exogenous H2O2, generating a high-refractive-index precipitate that significantly amplifies the SPR signal. The Zr-O-P coordination enables selective capture of phospholipid membranes on exosomes, while Fe3O4 satellites facilitate rapid magnetic enrichment and separation. To further improve specificity and antifouling performance, single-walled carbon nanotube interlayers pre-functionalized with PD-L1 targeting peptides were integrated onto the sensor chip, enabling selective recognition of magnetically enriched PD-L1+ exosomes. The combined refractive-index increase from the nanocomposite and the TMB deposition leads to enhanced SPR responses. Under optimized conditions, the assay achieves a detection limit of 2.16 particles mL-1 (S/N = 3) over a linear range of 102-107 particles mL-1. The total analysis time is within 40 min, and the method shows consistent differentiation between serum samples from cancer patients and healthy donors. This approach provides a practical strategy for the analysis of low abundance exosomal biomarkers.