CUSABIO Quarterly Citation Review: 800 New Product Citations in the First Quarter, Total Citations Hit 30,200!

This study reveals that thromboxane receptor TP in dendritic cells suppresses S100a8/a9 expression via PKCδ-Stat1 signaling, reducing neutrophil recruitment and NET formation to alleviate sepsis-induced lung injury. TP deficiency in DCs exacerbates sepsis, while DC-targeted TP agonist nanodrug improves outcomes.

This study developed an injectable hydrogel (EG-gel) via co-assembly of glycyrrhizic acid and embryonic stem cell-derived small extracellular vesicles. EG-gel exhibits self-healing, shear-thinning, and tissue adhesion, prolonging sEV retention at the injury site. GA provides early anti-inflammatory effects, while sEV promotes angiogenesis and neural repair, enabling a spatiotemporal “anti-inflammatory first, repair second” strategy that significantly improves functional recovery in TBI mice.

This study reveals that peritumoural adipose tissue secretes kynurenine, which is metabolized to 3-hydroxykynurenine in cancer cells. 3-HK directly binds NCOA4 to inhibit ferritinophagy, causing ferritin accumulation and reduced labile iron, thereby conferring ferroptosis resistance and impairing anti-PD-1 efficacy. Targeting the kynurenine pathway restores ferroptosis sensitivity and enhances immunotherapy.

This study identified TDRD9 upregulation in neutrophils from Pseudomonas aeruginosa pneumonia patients via RNA-seq. Mechanistically, TDRD9 suppresses neutrophil cuproptosis through the PD-L1/CD80/p38 MAPK axis, exacerbating lung injury. HA-modified siRNA nanoparticles targeting TDRD9 effectively induce neutrophil cuproptosis, reduce inflammation, and alleviate lung injury, with efficacy validated in human lung organoids, offering a promising therapeutic strategy for bacterial pneumonia.

This study identifies TCF21 as a key regulator in uterine development and endometriosis. Uterine-specific Tcf21 knockout in mice causes reduced endometrial thickness, stromal cell loss, and impaired fertility. Mechanistically, TCF21 activates LIMK2-cofilin signaling to promote cytoskeleton reorganization and EMT, enhancing stromal cell invasion and adhesion. TCF21 is highly expressed in ectopic lesions, and targeting LIMK2 effectively inhibits lesion growth, offering a potential therapeutic strategy for endometriosis.

This study identifies C/EBPβ as a transcription factor of FSHβ that directly binds its promoter to regulate expression. The AEP/C/EBPβ pathway upregulates postmenopausal FSHβ levels and induces osteoporosis. Knocking out C/EBPβ or AEP, or treating with AEP inhibitor #11a, suppresses FSHβ and alleviates osteoporosis in ovariectomized mice, with #11a showing efficacy comparable to FDA-approved teriparatide. TrkB agonists also counter osteoporosis but fail to reduce FSH due to no TrkB receptors in the pituitary. It reveals the AEP/C/EBPβ pathway as a novel therapeutic target for postmenopausal osteoporosis.

This study uses multi-omics and nanomechanics to reveal the dynamic remodeling and cross-species conservation of the ovarian matrisome during early follicular development. Integrin αvβ3 is identified as a key mediator of matrisome signals. Its inhibition has dual effects: promoting primordial follicle activation but inducing atresia, and impairing secondary follicle integrity and oocyte maturation. Similar collagen remodeling and stage-specific αvβ3 expression exist in human ovaries, providing new mechanisms and therapeutic targets for ovarian dysfunction and assisted reproductive technologies.

This study finds that very-long-chain ceramide Cer24:1 is significantly reduced in neutrophilic asthma (NA) patients, correlating with disease severity. Cer24:1 specifically binds EP2 receptor on CD4+T cells, inhibiting JAK2-STAT3 signaling pathway and RORγt-driven Th17 cell differentiation, thereby alleviating airway neutrophil infiltration and inflammation. Supplementing Cer24:1 mitigates symptoms in NA model mice, while PGE₂ competitively reverses its effects. These findings identify Cer24:1 as a novel metabolic regulator and provide a potential therapeutic strategy for steroid-resistant NA.

This study identifies M7core, a cGAS-STING pathway-driven gene signature, enabling quantitative assessment of pathway activity in systemic lupus erythematosus (SLE). M7core is activated in 70.4% of SLE samples, outperforms interferon-stimulated genes in diagnosis, and correlates with disease activity and lupus nephritis. STING antagonists suppress M7core and alleviate multi-organ pathology in model mice, while M7core gene ZBP1 deficiency exacerbates disease in specific models. It provides biomarkers and novel strategies for precise targeted therapy of SLE.

This study finds that elevated Irgm1 in neutrophils of myocardial infarction (MI) patients correlates with improved prognosis, while neutrophil-specific Irgm1 deletion exacerbates post-MI cardiac dysfunction. Mechanistically, Irgm1 interacts with PDIA3, promoting its autophagic degradation and activating the ER stress/NF-κB/caspase-3 pathway to facilitate neutrophil clearance and efferocytosis. PDIA3 inhibitor LOC14 reverses cardiac injury in Irgm1-deficient mice, identifying the Irgm1-PDIA3 axis as a novel therapeutic target and LOC14 a potential drug for MI.