Metabolic dysfunction-associated fatty liver disease is a common chronic liver disease worldwide， and its incidence rate continues to rise. The traditional “two-hit” theory has gradually been replaced by the “multiple-hit” hypothesis， which emphasizes the synergistic effect of multiple pathogenic factors. Necroptosis is an inflammatory form of death with both the morphological characteristics of necrosis and the signaling mechanism of apoptosis， and the core of necroptosis lies in the receptor-interacting protein kinase 1-receptor-interacting protein kinase 3-mixed lineage kinase domain-like pseudokinase signaling axis. This pathway directly leads to the death of hepatocytes， and it triggers an inflammatory response and promotes the fibrosis process by releasing damage-associated molecular patterns； the pathway is also closely associated with the metabolic reprogramming of the liver. This review summarizes the activation mechanism of necroptosis in metabolic dysfunction-associated fatty liver disease， analyzes its effect on liver inflammation， fibrosis， and metabolism， and explores its therapeutic strategies and application prospects.

Objective To investigate the effects of hemin on the quantity and apoptosis of human umbilical cord blood-derived late endothelial progenitor cells (EPCs) in vitro.Methods Mononuclear cells were isolated from human cord blood by density gradient centrifugation and were induced to differentiate to late EPCs in vitro.The second to third generation of attached late EPCs in good state were randomly plated for 24 h under different concentrations(0, 5, 10, 15 and 20 μmol/L)of hemin.Cell viability and proliferation were measured with typan blue staining and cell counting kit-8, respectively.Cell adhesion was analyzed by adhesive assay, and cell apoptosis was detected by flow cytometry.Results Compared to control group, hemin promoted viability of late EPCsat lower concentrations(5and 10μmol/L).Meanwhile, proliferation and adhesion were also improved and apoptosis was inhibited when the concentrations of hemin were 5,10, or 15 μ mol/L.All these effects were most prominent when hemin concentration was 10 μmoL/L, while the effects above were reversed when hemin concentration was moderated to 20 μmol/L.In addition, hemin showed a time-dependent manner in promoting cell proliferation and adhesion, and inhibiting apoptosis.That effects were most obvious at 24 h.Conclusions Lower concentration of herin augments the quantity and adhesion of late EPCs, inhibits cell apoptosis, while higher concentration present the reversed effects.