F13a1, also known as Coagulation Factor XIIIA, encodes a key molecule in blood coagulation [2]. It cross-links fibrin fibers and supports platelet adhesion in haemostasis, and is also involved in angiogenesis and tissue repair. FXIII promotes wound healing in multiple tissues through various plasma and cellular functions [2].

In human adipose tissue, F13A1 expression increases with acquired excess weight and is associated with the inflammatory status of adipocytes. Its differential expression in adipose tissue shows a negative correlation with circulating adiponectin and positive correlations with weight, body fat, and adipocyte size. A whole-transcriptome-wide association study identified 182 F13A1-associated genes involved in pathways like cell stress, inflammatory response, and tissue remodeling [1].

In septic patients, the expression of F13A1 in myeloid cells positively correlates with COVID-19 disease [3]. In multiple primary lung cancers (MPLCs), an immunosuppressive F13A1+ macrophage subtype is specifically enriched, which overexpresses M2 macrophage markers and is involved in shaping the immunosuppressive tumor microenvironment [4].

Congenital factor XIII deficiency is usually caused by mutations in the F13A1 gene. Various mutations in F13A1 have been identified in patients with this deficiency, such as missense, deletion, nonsense, and splice-site mutations [5,6,7,8,9].

In conclusion, F13a1 is crucial for blood coagulation, angiogenesis, and tissue repair. Studies on its role in obesity-related adipose tissue expansion and inflammation, sepsis, MPLCs, and factor XIII deficiency through genetic models help understand its functions in these biological processes and disease conditions. These findings may contribute to developing new therapeutic strategies for related diseases.