Porcine reproductive and respiratory syndrome (PRRS) is an infectious disease caused by the PRRS virus that leads to reproductive disorders and severe dyspnoea in pigs, which has serious economic impacts. One of the reasons PRRSV cannot be effectively controlled is that it has developed countermeasures against the host immune response, allowing it to survive and replicate for long periods. Transcription Factors acts as a bridge in the interactions between the host and PRRSV. PRRSV can create an environment conducive to PRRSV replication through transcription factors acting on miRNAs, inflammatory factors, and immune cells. Conversely, some transcription factors also inhibit PRRSV proliferation in the host. In this review, we systematically described how PRRSV uses host transcription factors such as SP1, CEBPB, STATs, and AP-1 to escape the host immune system. Determining the role of transcription factors in immune evasion and understanding the pathogenesis of PRRSV will help to develop new treatments for PRRSV.

Extracellular vesicles (EVs) have emerged as key mediators of intercellular communication at the maternal–fetal interface and play indispensable roles in the establishment and maintenance of pregnancy. This review provides a mechanistic perspective on how EV-mediated signaling coordinates physiological maternal–fetal communication and how disruption of these signaling networks contributes to pregnancy-related disorders. We summarize current evidence demonstrating that EVs regulate multiple complementary biological processes, including maternal immune tolerance, trophoblast adhesion and invasion, placental angiogenesis and vascular remodeling, epithelial–stromal crosstalk, and metabolic and inflammatory adaptation, thereby maintaining maternal–fetal homeostasis. We further discuss how dysregulated EV biogenesis, cargo composition, and intercellular communication contribute to the pathogenesis of preeclampsia, gestational diabetes mellitus, preterm birth, recurrent implantation failure, and fetal growth restriction. In addition, the potential applications of EV-associated molecules as non-invasive biomarkers and the emerging use of engineered EVs for targeted therapeutic delivery are critically evaluated. Particular emphasis is placed on current challenges that limit clinical translation, including methodological heterogeneity, lack of standardized isolation and characterization protocols, insufficient biomarker validation, and pregnancy-specific safety considerations. Overall, a deeper understanding of EV-mediated maternal–fetal communication, together with methodological standardization and rigorous clinical validation, will facilitate the development of reliable EV-based diagnostic and therapeutic strategies for pregnancy-related disorders.

The calpain proteolytic system plays a central role in cell death and cell signaling. Caspases are a family of proteases implicated in apoptosis. The objective of this study was to explore the...

The morphological diversity of sheep horns affects livestock production, yet its molecular regulation is poorly understood. COL7A1, essential for anchoring the epidermis to the dermis, was investigated using RNA-seq, WGS, and protein interaction prediction. COL7A1 was highly expressed in soft horn and skin, with higher levels in Scurred than Horned sheep (p < 0.05), suggesting a role in horn morphology. Cross-species alignment of 18 COL7A1 sequences revealed 15 amino acids unique to horned ruminants. RNA-seq and WGS identified four allele-specific expression (ASE) loci and 18 SNPs linked to horn traits. Two missense variants-SNP8 (p.Glu181Asp) and SNP14 (p.Ala2857Thr)-may alter protein structure, with SNP14 showing ASE. Kompetitive Allele-Specific PCR (KASP) genotyping of SNP4 and SNP8 confirmed associations with horn length (p < 0.05). Protein interaction modeling indicated COL7A1 synergizes with laminin γ2 (LAMC2), implicating basement membrane assembly. These results provided molecular insights into ovine horn development and support marker-assisted selection.

Embryo implantation is a highly selective and hormonally regulated event, critically dependent on endometrial receptivity and the molecular microenvironment of uterine fluid (UF). UF is actively secreted by endometrial glands and epithelial cells and comprises proteins, metabolites, hormones, and extracellular vesicles (EVs) carrying miRNAs, lncRNAs, and regulatory proteins. These components coordinate embryo development, trophoblast invasion, angiogenesis, and maternal–fetal immune tolerance. Dysregulation of UF composition is increasingly implicated in reproductive disorders, including recurrent implantation failure, unexplained infertility, endometriosis, adenomyosis, and polycystic ovary syndrome, highlighting its potential as a noninvasive biomarker of endometrial function. Despite advances, challenges remain in standardizing UF sampling, addressing temporal and inter-individual variability, and elucidating upstream regulatory networks. Integrative multi-omics analyses, functional organoid–embryo models, and longitudinal clinical studies are essential to translate UF insights into predictive diagnostics and therapeutic strategies, ultimately improving implantation success and reproductive outcomes.