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Table 1 The relationship between cell death and MAFLD

From: Targeting programmed cell death in metabolic dysfunction-associated fatty liver disease (MAFLD): a promising new therapy

Name

Relationship with MAFLD

Apoptosis

Intestinal barrier dysfunction, oxidative stress, and ER stress lead to lipoapoptosis and activate the external death receptor pathway and internal mitochondrial pathway

Glucose metabolism disorder activates the internal mitochondrial pathway and is regulated by several miRNAs

Necroptosis

Oxidative stress and intestinal barrier dysfunction trigger TNF-α-mediated necroptosis

The key molecule RIPK1 is involved in the regulation of RIPK3 function and in the mutual transformation with apoptosis

The interaction between RIPK3 and JNK is involved in disease progression, although the specific role is not clear

Inhibition of MLKL improves insulin resistance, regulates fat metabolism, etc

Pyroptosis

Intestinal barrier dysfunction, ER stress, and oxidative stress all activate the assembly of NLRP3, and the secretion of inflammatory factors IL-1β and IL-18 leads to pyroptosis

Ferroptosis

Imbalance in the intracellular antioxidant system caused by excessive iron deposition and oxidative stress leads to disorders of the ferroptosis regulatory system and further affects lipid accumulation, inflammation, liver fibrosis, etc

Autophagy

Autophagy affects insulin resistance, fat metabolism, inflammation, liver fibrosis, etc. by regulating ER stress, oxidative stress, etc