Skeletal muscle myogenesis and injury-induced muscle regeneration contribute to muscle formation and maintenance. As myogenic stem cells, skeletal muscle satellite cells have the ability to proliferate, differentiate and self-renew, and are involved in muscle formation and muscle injury repair. Accumulating evidence suggests that non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), are widely involved in the regulation of gene expression during skeletal muscle myogenesis, and their abnormal expression is associated with a variety of muscle diseases. From the perspective of the molecular mechanism and mode of action of ncRNAs in myogenesis, this review aims to summarize the role of ncRNAs in skeletal muscle satellite cells’ myogenic differentiation and in muscle disease, and systematically analyze the mechanism of ncRNAs in skeletal muscle development. This work will systematically summarize the role of ncRNAs in myogenesis and provide reference targets for the treatment of various muscle diseases, such as muscle dystrophy, atrophy and aberrant hypertrophy.

Interferon-γ (IFN-γ) is critical for innate and adaptive immunity against viral and bacterial infections. IFN-γ reportedly affects the phagocytic ability of monocytes and macrophages as well as regulates pituitary function in humans and mice. The present study analyzed the impact of IFN-γ on monocyte and macrophage phagocytosis, production performance, and pituitary function in vivo and in vitro (in dwarf chickens). IFN-γ was injected into dwarf chickens through a vein, and then, the laying rate, average egg weight, and levels of follicle-stimulating hormone (FSH) and IFN-γ were measured in treatment and control groups. For the in vitro experiment, the pituitary tissues were supplemented with IFN-γ, and the mRNA expression levels of follicle-stimulating hormone beta subunit (FSH-β), interferon gamma receptor 1 (IFNGR1), and interferon gamma receptor 2 (IFNGR2) in the pituitary were assessed. Monocyte and macrophage phagocytosis product (PP) was decreased by IFN-γ treatment in a dose-dependent manner in vitro. In the in vivo experiment, the level of IFN-γ in the treatment group was higher than that in the control group at 7 d (P < 0.05), 14 d (P < 0.01), and 21 d (P < 0.01) post-injection. Compared with the control group, monocyte and macrophage PP was lower in the treatment group after injection (P < 0.01). The laying rate was higher in the treatment group than in the control group at 2 and 3 wk post-injection (P < 0.05). There was a significant difference between the treatment and control groups in the levels of FSH at 1, 3, 7, and 14 d post-injection (P < 0.01). In the in vitro experiment, increased mRNA expression levels of FSH-β, IFNGR1, and IFNGR2 were observed in the treatment group after stimulation with 100 U/mL IFN-γ for 24 h compared to those in the control group (P < 0.05). IFN-γ inhibited the phagocytosis of monocytes and macrophages; up-regulated the mRNA expression levels of the FSH-β, IFNGR1, and IFNGR2; enhanced the secretion of FSH; and improved the laying rate. IFN-γ might be an important regulator in the trade-off between the immune effect and production performance in dwarf chickens.

Currently, a major challenge exists in CRISPR-mediated genome editing research in sheep: the low efficiency of exogenous large DNA fragment targeted integration without drug selection or fluorescence enrichment. This restriction significantly impedes the use of precise genome editing in sheep for agricultural, biological, and biomedical purposes. In this study, we employed the strategy of increasing the local concentration of the homologous repair template at the site of the DNA double-strand break (DSB). We achieved this by fusing the DNA binding domain (BD) of the Gal4 protein (Gal4-BD) to the N-terminal end of the SpCas9 protein using a 32-amino acid (aa) flexible linker. Additionally, we incorporated a 17 bp UAS at the 3′ end of the donor template, which can be specifically recognized and bound by Gal-BD. As a result, we observed a significant improvement in the knock-in efficiency of the exogenous large DNA fragment (2997 bp) in sheep fetal fibroblasts (SFFs), increasing it from 5.30% (8/151) to 16.67% (32/192), providing a comparatively efficient and user-friendly method to promote CRISPR-mediated gene knock-in in sheep.

Dengue fever (DF) is an acute mosquito-borne infectious disease caused by dengue virus (DENV), primarily transmitted by Aedes aegypti and Aedes albopictus. Nearly 4 billion people worldwide are at risk of infection, and the 2024 epidemic reached an unprecedented scale. Severe cases can lead to hemorrhage, shock, and even death, prompting the WHO to classify it as a potential pandemic pathogen. Current prevention and control measures face prominent bottlenecks, including limited applicable populations for vaccines, lack of specific antiviral drugs, and increasing insecticide resistance in mosquito vectors. Notably, susceptible animal models serve as core tools for elucidating the pathogenic mechanisms of dengue virus, screening antiviral drugs, and evaluating vaccine protective efficacy, holding irreplaceable significance. This review systematically summarizes the characteristics, application scenarios, and research progress of mainstream and potential susceptible animal models, including non-human primates, mice, pigs, tree shrews, and bats. It covers model systems with different immune statuses, genetically modified types, and species-specific traits. Among these, mouse models are the most widely used due to their high flexibility and controllable cost, while non-human primate models have become key carriers for preclinical vaccine evaluation by virtue of their high homology with human immune responses. However, current models generally suffer from core bottlenecks, such as incomplete simulation of core severe phenotypes, insufficient restoration of immune mechanisms, unclear viral receptor mechanisms, and lack of unified standards for inoculation doses and evaluation indicators. These limitations make it difficult to accurately replicate key severe disease mechanisms, including antibody-dependent enhancement (ADE) and cytokine storms. Future model development should focus on core requirements—including intact immunity, broad-spectrum susceptibility, and accurate simulation of clinical pathological features—prioritize solving the simulation challenges of ADE and cytokine storms, and establish standardized experimental systems and evaluation criteria. By comprehensively summarizing the advantages and limitations of the existing models, this review provides a systematic reference for the optimization and upgrading of dengue virus-susceptible animal models. It also holds important guiding significance for promoting the in-depth development of basic dengue research, innovation in prevention and control technologies, and clinical transformation and application.