Swap70, also known as Switch-associated protein 70, is a guanine nucleotide exchange factor involved in various cellular processes. It can interact with Rho-family GTPases, lipid phosphatidylinositol (3,4)-bisphosphate, and filamentous actin, playing roles in immunoregulation, cell maturation, and cell transformation [2,3,4]. It is also associated with pathways like mitogen-activated protein kinases signaling [1].

In cardiac hypertrophy, Swap70 knockout mice and knockdown cardiomyocytes experiments showed that Swap70 deficiency accelerates the progression of pathological cardiac hypertrophy, while overexpression restrains it. Swap70 suppresses cardiac hypertrophy possibly by inhibiting the mitogen-activated protein kinases signaling pathway in a TAK1-dependent manner [1].

In non-alcoholic fatty liver disease (NAFLD), hepatocyte-specific Swap70 knockout and overexpression mice fed a high-fat, high-cholesterol diet demonstrated that SWAP70 suppressed the progression of non-alcoholic steatohepatitis by inhibiting lipid accumulation, inflammatory response, and fibrosis, also through inhibiting the TAK1-related signaling [5].

In conclusion, Swap70 plays essential roles in multiple biological processes and diseases. The use of gene knockout mouse models has revealed its significance in pathological cardiac hypertrophy and NAFLD, mainly by modulating related signaling pathways, providing insights into the underlying mechanisms of these diseases and potential therapeutic targets.