Abstract
Calcium (Ca(2+)) is a second messenger for many signal pathways, and changes in intracellular Ca(2+) concentration ([Ca(2+)]i) are an important signaling mechanism in the oocyte maturation, activation, fertilization, function regulation of granulosa and cumulus cells and offspring development. Ca(2+) oscillations occur during oocyte maturation and fertilization, which are maintained by Ca(2+) stores and extracellular Ca(2+) ([Ca(2+)]e). Abnormalities in Ca(2+) signaling can affect the release of the first polar body, the first meiotic division, and chromosome and spindle morphology. Well-studied aspects of Ca(2+) signaling in the oocyte are oocyte activation and fertilization. Oocyte activation, driven by sperm-specific phospholipase PLCζ, is initiated by concerted intracellular patterns of Ca(2+) release, termed Ca(2+) oscillations. Ca(2+) oscillations persist for a long time during fertilization and are coordinately engaged by a variety of Ca(2+) channels, pumps, regulatory proteins and their partners. Calcium signaling also regulates granulosa and cumulus cells' function, which further affects oocyte maturation and fertilization outcome. Clinically, there are several physical and chemical options for treating fertilization failure through oocyte activation. Additionally, various exogenous compounds or drugs can cause ovarian dysfunction and female infertility by inducing abnormal Ca(2+) signaling or Ca(2+) dyshomeostasis in oocytes and granulosa cells. Therefore, the reproductive health risks caused by adverse stresses should arouse our attention. This review will systematically summarize the latest research progress on the aforementioned aspects and propose further research directions on calcium signaling in female reproduction.