Ribosomal proteins constitute the principal components of ribosomes, and their functions span a wide spectrum. Recent investigations have unveiled their involvement in oocyte and embryo development, playing a pivotal role in reproductive development. Numerous pieces of evidence indicate that ribosomal proteins participate in the regulation of various cellular activities, including nucleolar stress, oxidative stress, cell proliferation and autophagy. Despite these findings, the precise mechanisms through which ribosomal proteins influence reproductive development via these cellular activities remain elusive. Therefore, elucidating the mechanisms of action is essential for a comprehensive understanding of the role and function of ribosomal proteins in reproductive development. This paper systematically reviews the progress in research on nucleolar stress, oxidative stress, cell proliferation and autophagy concerning ribosomal proteins during reproductive development. Furthermore, we explore the potential of ribosomal proteins as diagnostic markers for various diseases. Additionally, we propose the development of drugs and therapies targeting ribosomal proteins, underscoring the potential for novel medical interventions in the context of reproductive health.

NIBV is an acute and highly contagious virus that has a major impact on the poultry industry. Wogonin, as a flavonoid drug, has antiviral effects, but there have been no reports indicating its role in renal injury caused by NIBV infection. The aim of this study is to investigate the antiviral effect of wogonin against NIBV. Renal tubular epithelial cells were isolated and cultured, and divided into four groups: Con, Con+Wog, NIBV and NIBV+Wog. We found that wogonin significantly inhibited the copy number of NIBV and significantly alleviated NIBV-induced cell apoptosis and necrosis. Moreover, wogonin inhibited the reduction in mitochondrial membrane potential and the aberrant opening of mPTP caused by NIBV. In conclusion, wogonin can protect renal tubular epithelial cells from damage by inhibiting the replication of NIBV and preventing mitochondrial apoptosis and necroptosis induced by NIBV.