MPO and metabolic dysfunction-associated steatohepatitis: In HFD-fed mouse models, CXCL1 [96], CXCR2 (induced via lipocalin-2) [97], and IL-8-mediated neutrophil infiltration have been shown to contribute to MASH pathogenesis through various mechanisms, including granule enzyme (e.g., MPO) and ROS release and increased activation of stress kinases [90, 98].