CUSABIO Quarterly Citation Review: 600 New Product Citations in the second Quarter, Total Citations Hit 31,400!

PRELP is downregulated in psoriatic lesions via IL-17A/STAT3-mediated transcriptional repression. PRELP suppresses keratinocyte proliferation, promotes apoptosis, inhibits NF-κB/MAPK signaling, and reduces IL-6/IL-23/IL-1β production, thereby limiting Th17 differentiation. Overexpression of PRELP alleviates psoriasiform dermatitis in mice, highlighting its role as an endogenous negative regulator of IL-17A-driven inflammation.

In MASLD, myeloid Mas interacts with PKM2 to enhance glycolysis and lactate production, driving Spi1 lactylation at K208. This promotes Spi1 nuclear translocation and transcriptional activation of SASP genes, fueling inflammatory senescence and disease progression. Macrophage membrane-coated nanoparticles delivering the Mas inhibitor TFDG effectively block this axis and ameliorate liver injury.

Hyocholic acids (HCAs), synthesized by fetal hepatic CYP3A7, constitute over 50% of meconium bile acids. HCAs promote Treg and suppress Th17 cell differentiation, shaping intestinal immune tolerance and facilitating healthy microbiome colonization. Neonates with higher HCA levels have reduced risks of infections and gastrointestinal disorders in the first year, revealing HCAs as a distinct primary bile acid critical for early-life immune programming.

The mevalonate pathway metabolite GGPP drives Tfh cell differentiation by enabling RAB35 geranylgeranylation, which sustains CXCR5 surface expression via endocytic recycling. TCR signaling enhances this axis through SREBP2, EGR1, and E2F1, and it is hyperactivated in lupus. Statins disrupt this pathway, ameliorating autoimmunity, revealing a metabolic vulnerability in Tfh-mediated diseases.

SFTSV infects the male reproductive tract in mice, targeting Leydig cells and inducing apoptosis and pyroptosis, leading to testosterone reduction and impaired spermatogenesis. scRNA-seq reveals CCR2⁺/SPP1⁺ macrophage-driven epididymal inflammation and fibrosis, which are alleviated by the S100A4 inhibitor niclosamide. Sexual transmission risk is suggested in mice, and clinical data show prolonged seminal viral shedding correlates with disease severity.

This study compared continuous-wave (CW) and 40 Hz transcranial photobiomodulation (tPBM) on 5xFAD AD mice. Both modalities rescued cognitive deficits via complementary glial pathways: CW preferentially activated astrocytes to strengthen gliovascular coupling for vascular and synaptic protection, while 40 Hz pulsed light mobilized microglia to surround and clear Aβ plaques, laying mechanistic foundation for precise AD phototherapy.

This work constructed streptavidin-assembled bifunctional nucleic acid nanoplatform DZ-G4/H NPs via RCA, integrating C1qa-targeted DNAzyme and peroxidase-mimicking G-quadruplex/hemin complex. It simultaneously breaks the vicious cycle of neuroinflammation and oxidative stress after TBI, alleviates cerebral edema, restores cerebral blood flow and cognitive/motor function, and offers a universal modular assembly strategy for multifunctional nucleic acid therapeutics.

This study finds reduced B. thetaiotaomicron in acute pancreatitis (AP) gut triggers PF4⁺ macrophage infiltration, recruiting neutrophils and Th2 cells via PF4-CCR1 axis to drive SIRS/CARS. B. thetaiotaomicron elevates intestinal NNMT to produce 1MNA, which binds ELF4 to suppress PF4 transcription and relieve inflammation. Two clinical cohorts verify fecal B. thetaiotaomicron, serum 1MNA and PF4 serve as severity biomarkers, offering microbiota-metabolism targeted therapies for AP.

This study built human thoracic aorta atlas via single-cell and spatial transcriptomics. AD patients lose elastic-support FBN1+ fibroblasts. Hypoxia triggers ENO1-mediated glycolytic reprogramming in VSMCs, which secretes MIF to retain and polarize pro-inflammatory M1 macrophages, degrading ECM. Lentiviral ENO1 knockdown alleviates aortic dissection in mice. ENO1-MIF axis and tranexamic acid are novel therapeutic candidates.

This study reveals cinnamaldehyde (CMA) restrains M1 macrophage glycolysis and pro-inflammatory polarization via BNIP3-dependent mitophagy. Macrophage membrane biomimetic nanoparticle MM@CMANP was fabricated to overcome poor solubility/bioavailability of CMA, targeting inflamed colon through CCR2. In DSS-induced IBD mice, MM@CMANP efficiently repairs intestinal barrier and alleviates colitis, offering targeted nanotherapy for inflammatory bowel disease.