2026-07-21T15:46:27Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/189162024-09-27T08:09:50Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Cicuéndez, Beatriz
author
Ruiz-Garrido, Irene
author
Mora, Alfonso
author
Sabio, Guadalupe
funder
Unión Europea. Comisión Europea. European Research Council (ERC)
funder
Fundación BBVA
funder
Ministerio de Economía y Competitividad (España)
funder
Asociación Española Contra el Cáncer
funder
Comunidad de Madrid (España)
funder
Ministerio de Ciencia, Innovación y Universidades (España)
funder
Fundación ProCNIC
2024-03-11T14:26:26Z
2024-03-11T14:26:26Z
2021-08
Mol Metab. 2021 Aug:50:101190.
10.1016/j.molmet.2021.101190
2212-8778
Molecular metabolism
33588102
http://hdl.handle.net/20.500.12105/18916
Non-alcoholic fatty liver disease (NAFLD) is an important component of metabolic syndrome and one of the most prevalent liver diseases worldwide. This disorder is closely linked to hepatic insulin resistance, lipotoxicity, and inflammation. Although the mechanisms that cause steatosis and chronic liver injury in NAFLD remain unclear, a key component of this process is the activation of stress-activated kinases (SAPKs), including p38 and JNK in the liver and immune system. This review summarizes findings which indicate that the dysregulation of stress kinases plays a fundamental role in the development of steatosis and are important players in inducing liver fibrosis. To avoid the development of steatohepatitis and liver cancer, SAPK activity must be tightly regulated not only in the hepatocytes but also in other tissues, including cells of the immune system. Possible cellular mechanisms of SAPK actions are discussed.
eng
Stress kinases in the development of liver steatosis and hepatocellular carcinoma.
review article
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URL
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Stress kinases_Mol Metab_2021.pdf
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Stress kinases_Mol Metab_2021.pdf.txt