F13a1, encoding coagulation factor XIII A subunit, is crucial in blood coagulation. It cross-links fibrin fibers, supports platelet adhesion, and is involved in angiogenesis and tissue repair pathways [2]. It also plays a role in adipogenesis, with implications for obesity-related adipose tissue expansion and inflammation [1].

In human adipose tissue, F13a1 mRNA expression significantly increases in individuals with acquired excess weight. Its differential expression shows a negative correlation with circulating adiponectin and positive correlations with weight, body fat, and adipocyte size. Transcriptome-wide association studies identify F13a1-associated genes in pathways like cell stress, inflammatory response, and extracellular matrix remodeling [1].

In multiple primary lung cancers, an immunosuppressive F13A1+ macrophage subtype is specifically enriched, which overexpresses M2 macrophage markers and is involved in shaping the immunosuppressive tumor microenvironment [3].

In conclusion, F13a1 is essential for blood coagulation, angiogenesis, and tissue repair. Its role in adipose tissue inflammation and obesity-related processes, as well as in the immunosuppressive tumor microenvironment of multiple primary lung cancers, has been revealed through human-based research. Understanding F13a1's functions provides insights into the mechanisms of these diseases and potential therapeutic targets.