Team players in the pathogenesis of metabolic dysfunctions-associated steatotic liver disease: The basis of development of pharmacotherapy

Figure 4 Activation of Ser/Thr kinases causes inhibitory phosphorylation on insulin-signaling molecules[35]. Lipotoxicity, inflammation, hyperglycemia, and subsequently oxidative stress, as well as mitochondrial dysfunction and endoplasmic reticulum stress, all converge on activation of Ser/Thr kinases, inducing inhibitory Ser/Thr phosphorylation of insulin receptor, insulin receptor substrate proteins, and Akt on multiple residues, causing insulin resistance. PKC: Protein kinase C; PKA: Protein kinase A; JNK: c-Jun N-terminal kinase; IKK: Inhibitor of nuclear factor-κB kinase; GSK: Glycogen synthase kinase 3. Citation: Boucher J, Kleinridders A, Kahn CR. Insulin receptor signaling in normal and insulin-resistant states. Cold Spring Harb Perspect Biol 2014; 6. Copyright © The Cold Spring Harbor Laboratory Press 2014. Published by Cold Spring Harbor Laboratory Press.