Nonalcoholic fatty liver disease is a common liver disease, and the incidence increases year by year. The pathogenesis of nonalcoholic fatty liver disease is correlated with insulin resistance and oxidative stress, which induces varied inflammatory cytokines (tumor necrosis factor-α, interleukin-1, interleukin-6, etc). Different signal transductions, such as mitogen-activated protein kinase, nuclear factor κB, activated protein kinase, Janus kinase 2/signal transducer and activator of transcription 3, peroxisome proliferator-activated receptor, phosphatidylinositol 3-kinase/protein kinase B, toll-like receptor, were activated by the pathogenic factors to regulate correlative reactions. Thus, an in-depth study of the signal transductions will probably provide new suitable solutions for the prevention and therapy of nonalcoholic fatty liver disease.
Sebastian, M. Signal transductions and nonalcoholic fatty liver. International Journal of Clinical Medical Research, 2024, 2, 44. https://doi.org/https://doi.org/10.61466/ijcmr2060004
AMA Style
Sebastian M. Signal transductions and nonalcoholic fatty liver. International Journal of Clinical Medical Research; 2024, 2(6):44. https://doi.org/https://doi.org/10.61466/ijcmr2060004
Chicago/Turabian Style
Sebastian, Michael 2024. "Signal transductions and nonalcoholic fatty liver" International Journal of Clinical Medical Research 2, no.6:44. https://doi.org/https://doi.org/10.61466/ijcmr2060004
APA style
Sebastian, M. (2024). Signal transductions and nonalcoholic fatty liver. International Journal of Clinical Medical Research, 2(6), 44. https://doi.org/https://doi.org/10.61466/ijcmr2060004
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