
-   Overexpression of CXCL1 increased mitochondrial metabolism and activated the epithelial-to-mesenchymal transition (EMT), which promoted hepatocellular carcinoma (HCC) progression. CXCL1 was identified as a direct target of miR- 200a, which inhibited CXCL1 expression post-transcriptionally in HCC. [PMID: 27542259].
-   IL-6 production is responsible for induction of hepatic gene expression of CXCL1 and CXCL8 in a rat model of septicemia produced by the intramuscular injection of turpentine oil (TO). The hepatic CXC-chemokines behaved like positive APPs that depend on IL6 production by activated macrophages recruited to extrahepatic damaged tissue [PMID: 35336843].
-   Ubiquitin specific peptidase 1 (USP1) upregulated SNAIL expression, leading to an increase in CXCL1 expression and promotes hepatic fibrosis in mice. The pro-fibrosis role caused by SNAIL upregulation was abolished by CXCL1 reduction [PMID: 33926817]. Elevated Cxcl1 expression levels were detected in hepatic fibrosis tissues, and Cxcl1 was verified as the downstream target gene of miR-150-5p [PMID: 33342075].
-   Hepatic overexpression of Cxcl1 contributed to the progression from steatosis to nonalcoholic steatohepatitis (NASH) by inducing neutrophil infiltration, oxidative stress, hepatocyte death, fibrosis, and the activation of p38 mitogen-activated protein kinase [PMID: 32937687].

## Summary

The CXCL1 gene encodes for CXC motif chemokine ligand 1, which functions as a chemoattractant for neutrophils, essential cells in the immune system's response to infection and injury [CS: 10]. CXCL1's chemotactic action is a crucial mechanism by which the body concentrates immune resources at sites of tissue damage or infection, facilitating the containment and elimination of pathogens as well as the removal of cell debris [CS: 9]. Its interaction with glycosaminoglycans (GAGs) modulates its binding and activity, implying a nuanced control of immune cell trafficking during the inflammatory response [CS: 8].

In kidney disease contexts such as sepsis-associated acute kidney injury (SA-AKI), CXCL1 emerges as a central hub gene, with its upregulation signifying an intensified effort by the body to recruit neutrophils to the injured kidney [CS: 8]. This response likely aims to curtail infection spread and contain the septic reaction [CS: 8]. However, while this recruitment is beneficial for acute immune defense, persistent or deregulated CXCL1 expression can lead to an exaggerated inflammatory reaction that exacerbates kidney damage [CS: 9]. Chronic or sustained activation of the Cxcl1 gene pathway, however, becomes maladaptive, given the potent effects of neutrophils which include the release of reactive oxygen species and proteases [CS: 9].
