Perimenopause is an important stage of female senescence. Epidemiological investigation has shown that the incidence of cardiovascular disease in premenopausal women is lower than that in men, and the incidence of cardiovascular disease in postmenopausal women is significantly higher than that in men. This phenomenon reveals that estrogen has a definite protective effect on the cardiovascular system. In the cardiovascular system, oxidative stress is considered important in the pathogenesis of atherosclerosis, myocardial dysfunction, cardiac hypertrophy, heart failure, and myocardial ischemia. From the perspective of oxidative stress, estrogen plays a regulatory role in the cardiovascular system through the estrogen receptor, providing strategies for the treatment of menopausal women with cardiovascular diseases.

Specific targeted drug delivery and controllable release of drugs at tumor regions are two of the main challenges for hepatocellular carcinoma (HCC) therapy, particularly post metastasis.

All eukaryotic cells contain the phospholipid phosphatidylinositol 4, 5-bisphosphate (PIP ₂ ) that serves multiple roles in signal transduction cascades. Type I phosphatidylinositol-4-phosphate 5-kinase (PIP5KI) catalyzes the synthesis of PIP ₂ by phosphorylating phosphatidylinositol 4 phosphate. Although the classical isoforms of PIP5KI (designated as α, β, and γ) all generate the same phospholipid product, they have significantly dissimilar primary structures and expression levels in different tissues, and they appear to localize within different compartments within the cell. Therefore, it appears likely that PIP5KI isoforms have overlapping, but not identical, functions. Here we show that targeted disruption of PIP5KIγ causes widespread developmental and cellular defects. PIP5KIγ-null embryos have myocardial developmental defects associated with impaired intracellular junctions that lead to heart failure and extensive prenatal lethality at embryonic day 11.5 of development. Loss of PIP5KIγ also results in neural tube closure defects that were associated with impaired PIP ₂ production, adhesion junction formation, and neuronal cell migration. These data, along with those of other PIP5KI isoforms, indicate that individual PIP5KI isoenzymes fulfill specific roles in embryonic development.