The silkworm (Bombyx mori) is an economically important insect that plays a crucial role in agricultural development. Antimony tin oxide, a high-tech multifunctional nanomaterial, is extensively utilized in contemporary industries due to its properties of transparency, conductivity, and stability. Nevertheless, the toxicity and potential adverse effects of antimony tin oxide on living organisms remain poorly understood. In this study, we evaluated the effects of antimony tin oxide at varying concentrations (0–3.2 μg/μL) on the growth, oxidative stress response, gene expression, and midgut integrity of fifth-instar silkworm larvae. Exposure to high concentrations of antimony tin oxide resulted in a significant reduction in larval weight and severely disrupted the antioxidant defense system. RNA sequencing (RNA-Seq) analysis identified 239 differentially expressed genes (DEGs), which were confirmed by qPCR, revealing up-regulated lipid synthesis gene AGPAT5, down-regulated chitin degradation gene Chi, and suppressed glycerolipid hydrolysis gene H9J6N7_BOMMO. Histopathological and ultrastructural examinations revealed severe damage to the structure of midgut epithelial cells. Structural and functional analysis of conserved domains in key DEG-encoded proteins revealed that gene dysregulation disrupted energy metabolism and compromised the physical barrier, ultimately linking molecular abnormalities to observed tissue damage. These findings elucidate the mechanisms by which antimony tin oxide induces midgut toxicity through interference with critical metabolic pathways and functional perturbations at the molecular level.

Spermatogenesis in Drosophila melanogaster is a classical model for studying cell polarity establishment, organelle remodeling, and extreme cellular morphogenesis. Spermatid elongation involves a series of highly coordinated dynamic events, including nuclear polarization, axonemal extension, mitochondrial remodeling, and individualization-mediated cytoplasmic clearance. Current studies have largely focused on individual structures, molecules, or pathways, resulting in a fragmented understanding of this process and a lack of an integrated framework that links mitochondrial function, cytoskeletal dynamics, and temporal translational regulation. Based on existing evidence, this review organizes current findings into three regulatory layers involving mitochondrial remodeling, cytoskeletal dynamics, and post-transcriptional translational control. Mitochondrial remodeling provides structural and metabolic support for sperm-tail formation, cytoskeletal processes execute axoneme organization and individualization, and post-transcriptional regulation controls the timing of protein production. Experimental evidence is strongest for mechanisms operating within each layer, whereas direct molecular coupling among the three layers remains incompletely established. We therefore present this model as a working framework rather than an established causal pathway. This framework helps organize current knowledge of extreme cellular differentiation and provides a basis for comparative studies of spermatogenesis and selected mechanisms associated with human male infertility.

This review presents a three-tiered engineering framework that systematically addresses these barriers. First, we survey chemical and sequence-based stabilization strategies, including lipidation, backbone N-methylation, and cyclization, that convert labile natural peptides into protease-resistant scaffolds. Second, moving beyond generic stabilization, we dissect the rational design of effector-inhibitory peptides, with particular emphasis on disulfide bond topology engineering as a powerful means to lock binding-competent conformations, alongside structure-guided interface optimization. Third, recognizing that purely rational design often fails to correctly fold complex topologies, we discuss complementary structure-constrained screening platforms (phage display, yeast display, and in silico docking) that exploit sequence–conformation coupling to enrich functional structures from vast libraries. Critically, we argue that these molecular-level designs can only achieve in vivo efficacy when co-integrated with delivery systems, including lipidic, polymeric, and viral carriers, which together determine bioavailability, targeting, and controlled release. By weaving these layers into a unified framework, we highlight a paradigm shift from sequential optimization toward context-aware co-design, where peptide rigidity, flexibility, affinity, and carrier compatibility are balanced against specific therapeutic or industrial contexts.