Pathogenesis of MetALD. Various molecular and cellular mechanisms contribute to the pathogenesis of MetALD. (IMAGE)

First Hospital of Jilin University

Pathogenesis of MetALD. Various molecular and cellular mechanisms contribute to the pathogenesis of MetALD.

Caption

The schematic images were created with BioRender (https://www.biorender.com/). ADH, alcohol dehydrogenase; ALDH2, aldehyde dehydrogenase 2; C1q, complement component 1q; ER, endoplasmic reticulum; FFA, free fatty acid; GCKR, glucokinase regulatory protein; HSC, hepatic stellate cell; IL-1β, interleukin 1β; IL-8, interleukin 8; MBOAT7, membrane-bound O-acyltransferase 7; MetALD, metabolic dysfunction and alcohol-associated liver disease; NET, neutrophil extracellular trap; NLRP3, NLR family pyrin domain containing 3; PNPLA3, patatin-like phospholipase domain-containing 3; RSPO3, R-spondin 3; S100A8, S100 calcium binding protein A8; TM6SF2, transmembrane 6 superfamily member 2; TREM2, triggering receptor expressed on myeloid cells 2. The schematic images were created with BioRender (https://www.biorender.com/).

Credit

By Bin Gao, Juan Pablo Arab, Suthat Liangpunsakul, et al.

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Credit must be given to the creator. Only noncommercial uses of the work are permitted.

License

CC BY-NC

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