Loss of RIP3 alleviates insulin resistance and inflammation in gestational diabetes mellitus mice via TLR4/MyD88/NF-κB signaling pathway - He, Yingying; Zhu, Weiwei; Qiu, Yuebo; Zhou, Kening (BMC pregnancy and childbirth, 2025)
Keywords: Animals; Cesarean section; Design of experiments; Diabetes, Gestational - genetics; Diabetes, Gestational - metabolism; Disease Models, Animal; Female; Gestational diabetes; Gestational diabetes mellitus; Glucose; Hypertension; Inflammation; Inflammation - genetics; Inflammation - metabolism; Insulin; Insulin resistance; Insulin Resistance - genetics; Insulin-Secreting Cells - metabolism; Kinases; Liver; Mice; Mice, Inbred C57BL; Myeloid Differentiation Factor 88 - metabolism; NF-kappa B - metabolism; Pregnancy; Proteins; Receptor-Interacting Protein Serine-Threonine Kinases - genetics; Receptor-Interacting Protein Serine-Threonine Kinases - metabolism; RIP3; Signal Transduction; TLR4/MyD88/NF-κB; Toll-Like Receptor 4 - metabolism; Variance analysis; United States--US; China; Shanghai China; TLR4/MyD88/NF-κB; Gestational diabetes mellitus; Insulin resistance; Inflammation; RIP3