Zfp30, a member of the KRAB-ZFP family, is a putative transcriptional repressor with a KRAB domain. It has been implicated in various biological processes.

In adipogenesis, it promotes the process by directly targeting and activating a retrotransposon-derived Pparg2 enhancer through recruitment of the co-regulator KAP1 [1]. In the context of non-alcoholic fatty liver disease (NAFLD), Zfp30 is significantly increased, and its silencing ameliorates lipid accumulation, while overexpression exacerbates triglyceride accumulation and steatosis in hepatocytes by down-regulating PPARα [2].

In a Zfp30 knockout mouse model, the null allele did not affect CXCL1 secretion or neutrophil recruitment to the lungs in response to innate immune stimuli. However, there was a significant reduction in the proportion of live Zfp30 homozygous female mutant mice from heterozygous matings, implicating Zfp30 in fertility or embryonic development [3]. Genetic studies in mice also suggest that Zfp30 is a regulator of neutrophilic airway inflammation, as a genetic variant in Zfp30 was found to regulate CXCL1 and neutrophil recruitment in a mouse model of house dust mite-induced asthma [4].

In conclusion, Zfp30 plays important roles in adipogenesis, NAFLD, and potentially in fertility or embryonic development as well as neutrophilic airway inflammation. The Zfp30 knockout mouse model has been valuable in revealing its functions in these biological processes and disease-related conditions, providing insights into the underlying molecular mechanisms.