Pork is a major global source of animal protein, and improving both its production efficiency and meat quality is a central goal in modern animal agriculture and food systems. This study investigated post-inflection-point growth patterns in two genetically distinct pig breeds—the lean-type Yorkshire pig (YP) and the fatty-type Qingyu pig (QYP)—with the aim of elucidating breed-specific characteristics that influence pork quality and yield. Comprehensive evaluations of carcass traits, meat quality attributes, nutritional composition, and gene expression profiles were conducted. After the growth inflection point, carcass traits exhibited greater variability than meat quality traits in both breeds, though with distinct patterns. YPs displayed superior muscle development, with the longissimus muscle area (LMA) increasing rapidly before plateauing at ~130 kg, whereas QYPs maintained more gradual but sustained muscle growth. In contrast, intramuscular fat (IMF)—a key determinant of meat flavor and texture—accumulated faster in YPs post inflection but plateaued earlier in QYPs. Correlation and clustering analyses revealed more synchronized regulation of meat quality traits in QYPs, while YPs showed greater trait variability. Gene expression patterns aligned with these phenotypic trends, highlighting distinct regulatory mechanisms for muscle and fat development in each breed. In addition, based on the growth curves, we calculated the peak age at which the growth rate declined in lean-type and fat-type pigs, which was approximately 200 days for YPs and around 270 days for QYPs. This suggests that these ages may represent the optimal slaughter times for the respective breeds, balancing both economic efficiency and meat quality. These findings provide valuable insights for enhancing pork quality through precision management and offer theoretical guidance for developing breed-specific feeding strategies, slaughter timing, and value-added pork production tailored to consumer preferences in the modern food market.

Ferroptosis is a new mode of cell death, which is characterized by inducing the accumulation of lipid peroxides dependent on iron ions and reactive oxygen species. It has been found that ferroptosis can lead to follicle atresia by promoting granulosa cell death and increasing its reactive oxygen species content, but the specific mechanism has not been elucidated. Through transcriptome sequencing, we found that ferroptosis markers and related genes were upregulated in porcine atretic follicles. PTGS2 was found to be differentially expressed between atretic and healthy follicles. By inhibiting NF-κB nuclear translocation, inhibition of the PTGS2 gene expression reduced the degree of ferroptosis in granulosa cells and rescued granulosa cell death and oxidative stress caused by ferroptosis. Therefore, we propose that the NF-κB/PTGS2 axis plays a key role in ferroptosis-induced granulosa cell death, leading to follicular atresia. Melatonin, a neurohormone secreted by the pineal gland of the upper thalamus, is involved in the regulation of various metabolic, immune, reproductive, and other processes. In the ferroptosis treatment group, melatonin treatment alleviated the degree of ferroptosis (downregulation of ferroptosis marker genes and markers) and decreased the expression of PTGS2. In summary, we have demonstrated that melatonin inhibits ferroptosis via the NF-κB/PTGS2 axis in granulosa cells.

Granulosa cell ferroptosis is a critical factor in follicular atresia and premature ovarian insufficiency (POI). As a regulated form of programmed cell death, ferroptosis is gaining significant attention in reproductive medicine research. MicroRNAs (miRNAs) play a crucial role in regulating key aspects of ferroptosis, including the glutathione-GPX4 pathway, glutamate/cystine transport, and iron and lipid metabolism. The present study demonstrates that miR-26a positively modulates ferroptosis by targeting SLC7A11, a member of the solute carrier family. We found that oocytes and granulosa cells are susceptible to the ferroptosis inducer erastin, and employed RNA sequencing to delineate the miRNA expression profiles during erastin-induced damage and ferroptosis. Notably, miR-26a expression was significantly upregulated in erastin-treated oocytes. Importantly, overexpression of miR-26a promoted ferroptosis in granulosa cells, while its knockdown inhibited this process. Ectopic miR-26a expression suppressed SLC7A11, thereby increasing ferroptosis. Our findings indicate that miR-26a influences ferroptosis by inhibiting glutathione synthesis, reducing cellular antioxidant capacity, and suggesting a potential strategy to enhance reproductive potential.

TRNA-derived small RNAs (tsRNAs) are emerging regulators of metabolism, but their roles in adipose tissue are not well defined. Here, we profiled tsRNA expression in mouse brown adipose tissue (BAT), gonadal white adipose tissues, and inguinal white adipose tissue (iWAT), revealing depot-specific patterns and a notable enrichment of mitochondrial tRF-5c fragments, especially tRF-1:29-chrM.Ser-GCT (tRF^Ser-GCT), in BAT. tRF^Ser-GCT expression correlated with mitochondrial abundance and increased during adipogenic differentiation and metabolic activation, both in vivo and in vitro. Functionally, tRF^Ser-GCT promoted adipogenesis and lipid accumulation in 3T3-L1 cells and localized to mitochondria. Mechanistically, tRF^Ser-GCT is generated from mitochondrial tRNA^Ser-GCT by the Ribonuclease P complex (Trmt10c, Hsd17b10, Prorp), with Hsd17b10 being essential for its biogenesis and for normal adipocyte lipid metabolism. tRF^Ser-GCT directly targets and downregulates Adrenoceptor Beta 2, a key metabolic regulator. In vivo, restoring tRF^Ser-GCT in Hsd17b10-deficient mice partially rescued adipose tissue accumulation and adipogenic gene expression. Together, these findings identify tRF^Ser-GCT as a mitochondrial tsRNA that promotes adipogenesis via the Ribonuclease P – Adrenoceptor Beta 2 axis, revealing a new layer of tsRNA-mediated regulation in adipose tissue biology.